JAX Mouse Strain Datasheet - 007084

B6.FVB(Cg)-Mmp9^tm1Tvu/J

Stock No:: 007084 |; MMP-9^-

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Overview

Also Known As: MMP-9^-

Because Mmp9^tm1Tvu homozygous mice show altered inflammatory responses they may be used to study injury response and repair, angiogenesis and inflammatory response.

Donating Investigator

IMR Colony, The Jackson Laboratory

Genetic overview

Genetic Background	Generation
	N8pN1F8 (18-AUG-17)

Mmp9^tm1Tvu

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Mmp9	matrix metallopeptidase 9

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Research Applications

Cardiovascular Research
Developmental Biology Research
Endocrine Deficiency Research
Immunology, Inflammation and Autoimmunity Research
Internal/Organ Research
Sensorineural Research
Cancer Research

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Base Price

Starting at:

$224.00 Domestic price for female

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Details

Detailed Description

Mice that are homozygous null for the Mmp9 (matrix metalloproteinase 9) gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of three-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (six to eight times larger vs. wild-type) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by eight weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development

A targeting vector containing a neomycin resistance gene driven by the mouse phosphoglycerate kinase promoter was used to disrupt a most of exon 2 and all of intron 2 of the Mmp9 gene. The construct was electroporated into 129S-derived ZW4 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric male animals were mated with Swiss Black females. Progeny animals were mated to Black Swiss mice for an unknown number of generations before being mated with FVB/N animals. Upon arrival at The Jackson Laboratory mice, were mated to C57BL/6J animals for a minimum of N5 generations.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Coussens LM; Tinkle CL; Hanahan D; Werb Z. 2000. MMP-9 supplied by bone marrow-derived cells contributes to skin carcinogenesis. In: . . MGI: J:65699

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Genetics

Mmp9^tm1Tvu

Allele Symbol: Mmp9^tm1Tvu

Allele Name	targeted mutation 1, Thiennu H Vu
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	GelB^-; Gelatinase B-Null; MMP-9 KO; MMP-9^-; MMP-9KO; MMP9^-; Mmp9-
Gene Symbol and Name	Mmp9, matrix metallopeptidase 9
Gene Synonym(s)	AW743869; B/MMP9; CLG4B; Clg4b; Clg4b; GELB; Gel B; Gelatinase B; MANDP2; MMP-9; collagenase IVB, basement membrane, 92 kDa; expressed sequence AW743869; gelatinase B
Strain of Origin	129S6/SvEvTac
Chromosome	2
General Note	ES cell line = ZW4.
Molecular Note	Part of exon 2 and all of intron 2 were replaced with a cassette containing the neomycin resistance gene driven by a PGK promoter.
Mutations Made By	Zena Werb, University of California, San Francisco

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Cardiovascular Research
- Ischemia studies
Developmental Biology Research
- Defects in Extracellular Matrix Molecules
- Skeletal Defects
Endocrine Deficiency Research
- Bone/Bone Marrow Defects
Immunology, Inflammation and Autoimmunity Research
- Inflammation
Internal/Organ Research
- Skeleton
Sensorineural Research
- Nociception

Genotype: Mmp9^tm1Tvu related

Cancer Research
- Increased Tumor Incidence
  - Skin Cancers
  - Skin Cancers: Resistant
Developmental Biology Research
- Defects in Extracellular Matrix Molecules
Endocrine Deficiency Research
- Bone/Bone Marrow Defects
Immunology, Inflammation and Autoimmunity Research
- Inflammation

Mammalian Phenotype Terms by Genotype

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
B6.129S6-Mmp9^tm1Tvu

neoplasm

abnormal tumor morphology
- injected A549 cells exhibit an increase in early apoptosis compared to in wild-type mice

decreased tumor incidence
- mice injected with Lewis lung carcinoma or A549 cells exhibit a decrease in tumors compared with similarly treated wild-type mice

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
either: (involves: 129S6/SvEvTac) or (involves: 129S6/SvEvTac * C57BL/6J)

cardiovascular system phenotype

abnormal angiogenesis
- exhibit reduced angiogenic response to peripheral leg ischemia; do not observe an increase in capillary density and see reduced capillary perfusion capacity and fewer points of capillary intersections (decreased branching) after ischemia

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * C57BL/6J

cardiovascular system phenotype

abnormal angiogenesis
- exhibit significantly reduced carotid artery intimal hyperplasia in response to vascular injury and fewer intimal smooth muscle cells

abnormal vascular smooth muscle physiology
- exhibit impairment of smooth muscle cell migration through a gelatin-coated membrane towards a chemoattractant and in a wound assay4
- isolated smooth muscle cells exhibit impaired ability to compact collagen gels, to assemble fibrillar collagen from exogenous monomers, and to attach to gelatin

muscle phenotype

abnormal vascular smooth muscle physiology
- exhibit impairment of smooth muscle cell migration through a gelatin-coated membrane towards a chemoattractant and in a wound assay4
- isolated smooth muscle cells exhibit impaired ability to compact collagen gels, to assemble fibrillar collagen from exogenous monomers, and to attach to gelatin

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * C57BL/6

immune system phenotype

abnormal chemokine level
- however, mice exhibit normal levels of CCL2, CCL3, and CCL5 following ovalbumin treatment
- on day 24, alum treated mice exhibit an increase in CCL22 in lung tissue compared with similarly treated wild-type mice
- on day 24, ovalbumin-treated mice exhibit an increase in bronchoalveolar lavage CCL22 compared with similarly treated wild-type mice
- on day 30, ovalbumin-treated mice exhibit an increase in lung tissue CCL22 compared with similarly treated wild-type mice
- on days 24 and 30, ovalbumin-treated mice exhibit increased CCL11 in the bronchoalveolar lavage compared with similarly treated wild-type mice

abnormal cytokine secretion

abnormal leukocyte morphology

abnormal response to infection
- in experimental peritonitis, mice exhibit higher spleen bacterial titers compared with similarly treated wild-type mice
- mice infected with Streptoccocus pneumoniae to in the right forebrain exhibit higher blood and spleen bacterial titers compared with similarly treated wild-type mice

decreased interferon-gamma secretion
- ovalbumin-treated mice exhibit decreased IFN-gamma in bronchoalveolar lavage compared with similarly treated wild-type mice

increased IgE level
- ovalbumin-treated mice exhibit increased ovalbumin-IgE compared with similarly treated wild-type mice

increased T cell proliferation
- on day 24 hours in ovalbumin-treated wild-type mice compared with similarly treated wild-type mice

increased T-helper 2 cell number
- on day 24, ovalbumin-treated mice exhibit an increased in Th2 helper cells in the bronchoalveolar lavage compared with similarly treated wild-type mice

increased eosinophil cell number
- on days 24 and 30, ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue eosinophil numbers compared with similarly treated wild-type mice

increased interferon-gamma secretion
- on day 24, T cells from alum-treated mice exhibit increased IFN-gamma secretion compared with cells from similarly treated wild-type mice

increased interleukin-13 secretion
- ovalbumin-treated mice exhibit increased IL13 in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice

increased interleukin-4 secretion
- on day 24, T cells from ovalbumin-treated mice exhibit increased IL4 secretion compared with cells from similarly treated wild-type mice
- ovalbumin-treated mice exhibit increased IL4 in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice

increased interleukin-5 secretion
- ovalbumin-treated mice exhibit increased IL5 in lung tissue compared with similarly treated wild-type mice

increased lymphocyte cell number
- ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue lymphocyte numbers compared with similarly treated wild-type mice

increased macrophage cell number
- ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue macrophage cell numbers compared with similarly treated wild-type mice

increased monocyte cell number
- ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue monocyte numbers compared with similarly treated wild-type mice

lung inflammation
- ovalbumin-treated mice exhibit increased lung inflammation with increased total cells, eosinophils, macrophages, lymphocytes, and monocytes in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice

homeostasis/metabolism phenotype

abnormal chemokine level
- however, mice exhibit normal levels of CCL2, CCL3, and CCL5 following ovalbumin treatment
- on day 24, alum treated mice exhibit an increase in CCL22 in lung tissue compared with similarly treated wild-type mice
- on day 24, ovalbumin-treated mice exhibit an increase in bronchoalveolar lavage CCL22 compared with similarly treated wild-type mice
- on day 30, ovalbumin-treated mice exhibit an increase in lung tissue CCL22 compared with similarly treated wild-type mice
- on days 24 and 30, ovalbumin-treated mice exhibit increased CCL11 in the bronchoalveolar lavage compared with similarly treated wild-type mice

respiratory system phenotype

lung inflammation
- ovalbumin-treated mice exhibit increased lung inflammation with increased total cells, eosinophils, macrophages, lymphocytes, and monocytes in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice

hematopoietic system phenotype

abnormal leukocyte morphology

increased IgE level
- ovalbumin-treated mice exhibit increased ovalbumin-IgE compared with similarly treated wild-type mice

increased T cell proliferation
- on day 24 hours in ovalbumin-treated wild-type mice compared with similarly treated wild-type mice

increased T-helper 2 cell number
- on day 24, ovalbumin-treated mice exhibit an increased in Th2 helper cells in the bronchoalveolar lavage compared with similarly treated wild-type mice

increased eosinophil cell number
- on days 24 and 30, ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue eosinophil numbers compared with similarly treated wild-type mice

increased lymphocyte cell number
- ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue lymphocyte numbers compared with similarly treated wild-type mice

increased macrophage cell number
- ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue macrophage cell numbers compared with similarly treated wild-type mice

increased monocyte cell number
- ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue monocyte numbers compared with similarly treated wild-type mice

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
either: (involves: 129S6/SvEvTac * Black Swiss) or (involves: 129S6/SvEvTac * CD-1)

skeleton phenotype

abnormal long bone epiphyseal plate morphology
- abnormal growth plate development, however after 3 weeks of age, aberrant apoptosis, vascularization, and ossification compensate to remodel the enlarged growth plate and ultimately produce an axial skeleton of normal appearance except for the shorter long bonesg bones

abnormal long bone hypertrophic chondrocyte zone
- apoptosis of hypertrophic chondrocytes is delayed
- by 3 weeks of age, when the hypertrophic zone is lengthened, aberrant apoptosis begins in the middle of the hypertrophic cartilage and is seen around the areas of ossification throughout the hypertrophic zone at 4 weeks
- ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age

abnormal metatarsal bone morphology
- hypertrophic cartilage zone in the metatarsals is about twice that of wild-type at birth and becomes more pronounced with growth so that by 3 weeks, it is 6-8 times as long

abnormal trabecular bone morphology
- area of metaphyseal trabecular bone is shorter

decreased length of long bones
- long bones are about 10% shorter than in wild-type

delayed bone ossification
- secondary (epiphyseal) ossification sites are delayed until 2.5 weeks of age, however, by 3 weeks of age, these sites are completely ossified as in wild-type

increased width of hypertrophic chondrocyte zone
- exhibit lengthened zone of hypertrophic cartilage with no difference in the reserve or proliferating zones

osteopetrosis
- ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age and the ectopic ossification proceeds rapidly so that in some bones the entire zone of hypertrophic cartilage is ossified, leading to a large area of trabecular bone, however this is resolved with subsequent remodeling so that by 8 weeks, bones appear normalone, however this is resolved with subsequent remodeling so that by 8 weeks, bones appear normal

short femur

short tibia

limbs/digits/tail phenotype

abnormal metatarsal bone morphology
- hypertrophic cartilage zone in the metatarsals is about twice that of wild-type at birth and becomes more pronounced with growth so that by 3 weeks, it is 6-8 times as long

short femur

short tibia

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
either: FVB.129S6-Mmp9^tm1Tvu or (involves: 129S6/SvEvTac)

cardiovascular system phenotype

altered response to myocardial infarction
- exhibit less left ventricular dilation after experimental myocardial infarction and show less collagen accumulation in the infracted area than seen in wild-type

homeostasis/metabolism phenotype

altered response to myocardial infarction
- exhibit less left ventricular dilation after experimental myocardial infarction and show less collagen accumulation in the infracted area than seen in wild-type

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129/Sv * 129S6/SvEvTac

homeostasis/metabolism phenotype

decreased circulating interleukin-10 level
- DNFB-sensitized and challenged mice have lower IL10 levels compared with similarly treated wild-type mice despite normal capacity of spleen cells to produce IL10 after LPS exposure

immune system phenotype

decreased circulating interleukin-10 level
- DNFB-sensitized and challenged mice have lower IL10 levels compared with similarly treated wild-type mice despite normal capacity of spleen cells to produce IL10 after LPS exposure

increased susceptibility to type IV hypersensitivity reaction
- DNFB-sensitized and challenged mice exhibit a prolonged response and delayed resolution of inflammation compared with similarly treated wild-type mice
- however, resolution of phenol elicited inflammation is normal

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * FVB/N

nervous system phenotype

decreased neuron apoptosis
- wild-type neurons co-cultured with microglial cells exposed to TFN-alpha exhibit decreased cell death compared to neurons co-cultured with similarly treated wild-type microglial cells

homeostasis/metabolism phenotype

delayed wound healing
- at days 3, 5, and 7, mice exhibit delayed wound compared with similarly treated wild-type mice

cellular phenotype

decreased neuron apoptosis
- wild-type neurons co-cultured with microglial cells exposed to TFN-alpha exhibit decreased cell death compared to neurons co-cultured with similarly treated wild-type microglial cells

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
FVB.129S6-Mmp9^tm1Tvu

mortality/aging

decreased sensitivity to xenobiotic induced morbidity/mortality
- DSS-treated mice exhibit no mortality unlike similarly treated wild-type mice
- however, mice exhibit normal mortality in response to Salmonella typhimurium-induced systemic sepsis

cardiovascular system phenotype

abnormal physiological neovascularization
- exhibit increased neovascularization post myocardial infarction, as shown by increased total vessel density and normalized vessel distribution between subendo- and epicardial regions relative to wild-type after coronary artery ligation

altered response to myocardial infarction
- exhibit an increased infarct-to-septal wall thickness ratio, attenuated wall thinning, improved left ventricular function, and reduced peak macrophage infiltration into the infarct zone relative to wild-type after myocardial infarction

increased angiogenesis
- exhibit an increased angiogenic potential after myocardial infarction, as shown by the presence of newly formed vessels in the infarct region

increased ventricle muscle contractility
- exhibit higher end-systolic pressure and dP/dt_max than wild-type after myocardial infarction, despite similar infarct sizes

immune system phenotype

abnormal neutrophil physiology
- neutrophil chemotatic response to fMLP is greater than for wild-type cells
- polymononuclear cell migration through Matri-gel-coated membrane in response to fMLP is greater compared with similarly treated wild-type cells

decreased susceptibility to induced colitis
- DSS-treated mice exhibit no weight loss, mortality or lymphocyte accumulation in the colon, reduced neutrophil accumulation, colon shortening, intestinal inflammation, and intestinal injury, and fewer incidence of diarrhea and bleeding compared with similarly treated wild-type micearly treated wild-type mice
- mice treated orally with Salmonella typhimurium to induce colitis exhibit reduced weight loss and destruction of crypt architecture compared with similarly treated wild-type mice

immune system phenotype

homeostasis/metabolism phenotype

altered response to myocardial infarction
- exhibit an increased infarct-to-septal wall thickness ratio, attenuated wall thinning, improved left ventricular function, and reduced peak macrophage infiltration into the infarct zone relative to wild-type after myocardial infarction

decreased sensitivity to xenobiotic induced morbidity/mortality
- DSS-treated mice exhibit no mortality unlike similarly treated wild-type mice
- however, mice exhibit normal mortality in response to Salmonella typhimurium-induced systemic sepsis

muscle phenotype

increased ventricle muscle contractility
- exhibit higher end-systolic pressure and dP/dt_max than wild-type after myocardial infarction, despite similar infarct sizes

digestive/alimentary phenotype

decreased susceptibility to induced colitis
- DSS-treated mice exhibit no weight loss, mortality or lymphocyte accumulation in the colon, reduced neutrophil accumulation, colon shortening, intestinal inflammation, and intestinal injury, and fewer incidence of diarrhea and bleeding compared with similarly treated wild-type micearly treated wild-type mice
- mice treated orally with Salmonella typhimurium to induce colitis exhibit reduced weight loss and destruction of crypt architecture compared with similarly treated wild-type mice

hematopoietic system phenotype

abnormal neutrophil physiology
- neutrophil chemotatic response to fMLP is greater than for wild-type cells
- polymononuclear cell migration through Matri-gel-coated membrane in response to fMLP is greater compared with similarly treated wild-type cells

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
C3N.129S6-Mmp9^tm1Tvu

immune system phenotype

decreased susceptibility to bacterial infection
- however, mice exhibit normal development of carditis when infected with B. burgdorferi
- mice infected with Borrelia burgdorferi exhibit less ankle swelling, joint inflammation, and arthritis than similarly treated wild-type mice

decreased susceptibility to induced arthritis
- B. burgdorferi-infected mice exhibit reduced arthritis compared with similarly treated wild-type mice
- however, spirochete numbers in the joint are normal

joint inflammation
- in B. burgdorferi-infected mice compared with similarly treated wild-type mice

skeleton phenotype

decreased susceptibility to induced arthritis
- B. burgdorferi-infected mice exhibit reduced arthritis compared with similarly treated wild-type mice
- however, spirochete numbers in the joint are normal

joint inflammation
- in B. burgdorferi-infected mice compared with similarly treated wild-type mice

joint swelling
- in B. burgdorferi-infected mice compared with similarly treated wild-type mice

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
FVB.Cg-Mmp9^tm1Tvu/J

mortality/aging

decreased susceptibility to viral infection induced morbidity/mortality
- however, mice exhibit a normal survival when injected intracerebrally with West Nile virus
- mice infected with West Nile virus exhibit decreased mortality compared with similarly treated wild-type mice

integument phenotype

hypoalgesia
- 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice
- however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation

immune system phenotype

decreased susceptibility to viral infection
- however, mice exhibit a normal response to West Nile virus infection when injected intracerebrally with the virus
- mice infected with West Nile virus exhibit decreased mortality, brain viral load, CD45+ leukocyte infiltration into brain tissue, and blood brain barrier permeability compared with similarly treated wild-type mice

decreased susceptibility to viral infection induced morbidity/mortality
- however, mice exhibit a normal survival when injected intracerebrally with West Nile virus
- mice infected with West Nile virus exhibit decreased mortality compared with similarly treated wild-type mice

digestive/alimentary phenotype

abnormal intestinal goblet cell morphology
- however, the number of goblet cells per crypt is normal
- mice exhibit an increased in the number of intestinal goblet cells compared to in wild-type mice

behavior/neurological phenotype

hypoalgesia
- 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice
- however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation

homeostasis/metabolism phenotype

abnormal response/metabolism to endogenous compounds
- mice treated with tumor necrosis factor-related weak inducer of apoptosis (TWEAK or Tnfsf12) exhibit increased body and muscle weight, intact basement membrane, and reduced myopathy, clustering of inflammatory cells, and number of necrotic fibers in the muscle compared with similarly treated wild-type miceuscle compared with similarly treated wild-type mice

decreased susceptibility to injury
- 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice
- following hepatic ischemia and reperfusion, hepatic apoptosis is decreased compared to in similarly treated wild-type mice
- however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation

cardiovascular system phenotype

abnormal blood-brain barrier function
- mice infected with West Nile virus exhibit decreased blood brain barrier permeability compared with similarly treated wild-type mice

nervous system phenotype

abnormal blood-brain barrier function
- mice infected with West Nile virus exhibit decreased blood brain barrier permeability compared with similarly treated wild-type mice

growth/size/body region phenotype

increased body weight
- in tumor necrosis factor-related weak inducer of apoptosis (TWEAK or Tnfsf12)-treated mice compared with similarly treated wild-type mice

muscle phenotype

increased tibialis anterior weight
- the weight of the tibialis anterior in mice treated with Tnfsf12-treated mice is greater than in similarly treated wild-type mice

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
129S6/SvEvTac-Mmp9^tm1Tvu

immune system phenotype

immune system phenotype
- mice exhibit a normal local Shwartman response namely thrombohemorrhagic vasculitis

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NTac

behavior/neurological phenotype

impaired contextual conditioning behavior
- however, mice tested at 30 hours for cued conditioning is normal
- when tested at 24 hours, mice exhibit reduced memory in hippocampus-dependent context conditioning compared with similarly treated wild-type mice

nervous system phenotype

reduced long term potentiation
- however, mice exhibit normal NMDA receptor-dependent long term depression and paired pulse facilitation
- long term potentiation is smaller in magnitude and shorter in duration than in wild-type mice

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * CD-1

mortality/aging

increased sensitivity to xenobiotic induced morbidity/mortality
- following myelodepletion with 5-fluorouracil (5-FU), 72% of mice die unlike similarly treated wild-type mice

hematopoietic system phenotype

abnormal bone marrow cell physiology
- in transplantation experiments, chemokine-induced mobilization of bone marrow repopulating cells is impaired compared to in similarly treated wild-type mice
- mobilization of bone-marrow derived circulating endothelial cell progenitors is impaired compared to in similarly treated wild-type mice

abnormal hematopoietic stem cell morphology
- following myelodepletion with 5-fluorouracil (5-FU), fewer hematopoietic stem cells enter S phase compared to in similarly treated wild-type mice

abnormal megakaryocyte differentiation
- restoration of myeloid and megakaryotic lineages in 5-FU-treated mice is impaired compared to in similarly treated wild-type mice

impaired hematopoiesis
- following myelodepletion with 5-fluorouracil (5-FU), mice exhibit delayed recovery compared with similarly treated wild-type mice

impaired myelopoiesis
- restoration of myeloid and megakaryotic lineages in 5-FU-treated mice is impaired compared to in similarly treated wild-type mice

homeostasis/metabolism phenotype

decreased susceptibility to injury
- following optic nerve ligation, retinas fail to exhibit apoptosis unlike in similarly treated wild-type mice

decreased susceptibility to ischemic brain injury
- 24 hours following cerebral ischemia, mice exhibit reduced ischemic lesion volumes compared with similarly treated wild-type mice
- however, mice subjected to cerebral ischemia exhibit normal neurological deficits

increased sensitivity to xenobiotic induced morbidity/mortality
- following myelodepletion with 5-fluorouracil (5-FU), 72% of mice die unlike similarly treated wild-type mice

nervous system phenotype

decreased susceptibility to ischemic brain injury
- 24 hours following cerebral ischemia, mice exhibit reduced ischemic lesion volumes compared with similarly treated wild-type mice
- however, mice subjected to cerebral ischemia exhibit normal neurological deficits

immune system phenotype

impaired myelopoiesis
- restoration of myeloid and megakaryotic lineages in 5-FU-treated mice is impaired compared to in similarly treated wild-type mice

vision/eye phenotype

abnormal retinal apoptosis
- following optic nerve ligation, retinas fail to exhibit apoptosis unlike in similarly treated wild-type mice

cellular phenotype

abnormal megakaryocyte differentiation
- restoration of myeloid and megakaryotic lineages in 5-FU-treated mice is impaired compared to in similarly treated wild-type mice

abnormal retinal apoptosis
- following optic nerve ligation, retinas fail to exhibit apoptosis unlike in similarly treated wild-type mice

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac

mortality/aging

increased susceptibility to viral infection induced morbidity/mortality
- CVB3-infected mice exhibit increased morbidity compared with similarly treated wild-type mice

homeostasis/metabolism phenotype

abnormal chemokine level
- ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice

abnormal vascular wound healing
- exhibit attenuated arterial remodeling in response to vascular injury (ligation of carotid artery) compared to wild-type, with decreases in late lumen loss, neointimal thickening, and migration of smooth muscle cells into the neointima and an accumulation of interstitial collagen of interstitial collagen

decreased physiological sensitivity to xenobiotic
- following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice
- mice sensitized and exposed to ovalbumin exhibit impaired ovalbumin-IgE production compared with similarly treated wild-type mice
- mice sensitized and exposed to ovalbumin fail to exhibit the airway inflammation observed in similarly treated wild-type mice
- ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice

decreased susceptibility to injury
- following IgG-induction of acute lung injury, mice exhibit reduced lung injury, decreased BALF protein leakage, and perivascular edema compared with similarly treated wild-type mice
- following induction of aortic aneurysm with elastase, mice develop fewer aneurysms with less of an increase in aortic diameter compared with similarly treated wild-type mice
- however, mice reconstituted with wild-type bone marrow exhibit normal susceptibility to elastase-induced aortic aneurysms
- however, mice reconstituted with wild-type neutrophils exhibit normal response to anti-Col17a1 antibodies
- however, the number of macrophages and neutrophils recruited to the lungs is normal in mice with IgG-induced acute lung injury
- mice are resistant to the pathogenic activity of anti-mBP180 (Col17a1) antibodies that induce subepidermal blistering in wild-type mice
- mice are resistant to traumatic brain injury compared with similarly treated wild-type mice with smaller traumatic lesion volumes

increased circulating interferon-beta level
- in CVB3-infected mice compared to in similarly treated wild-type mice

increased circulating interferon-gamma level
- in CVB3-infected mice compared to in similarly treated wild-type mice

immune system phenotype

abnormal Langerhans cell physiology
- however, maturation of Langerhans cells is normal
- migration of Langerhans cells is impaired compared to in wild-type mice

abnormal chemokine level
- ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice

abnormal dendritic cell physiology
- however, homing of dendritic cells from airways to lymph nodes in mice is normal
- in vitro, chemotaxis of dendritic cells in response to CCL5 (RANTES) and CCL20 (MIP-3alpha) is impaired compared with similarly treated wild-type cells

decreased IgE level
- mice sensitized and exposed to ovalbumin exhibit impaired ovalbumin-IgE production compared with similarly treated wild-type mice

decreased dendritic cell number
- following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice

decreased inflammatory response
- mice sensitized and exposed to ovalbumin fail to exhibit the airway inflammation observed in similarly treated wild-type mice

increased circulating interferon-beta level
- in CVB3-infected mice compared to in similarly treated wild-type mice

increased circulating interferon-gamma level
- in CVB3-infected mice compared to in similarly treated wild-type mice

increased susceptibility to viral infection
- Coxsackievirus B3 (CVB3)-infected mice exhibit increased morbidity, viral load, serum IFN-gamma and IFN-beta, left ventricular posterior wall and interventricular septum thickness, and cardiac injury as determined by increased myocytolysis, calcification, and cellular infiltrate and decreased ejection fraction and E wave compared with similarly treated wild-type mice, and cellular infiltrate and decreased ejection fraction and E wave compared with similarly treated wild-type mice

increased susceptibility to viral infection induced morbidity/mortality
- CVB3-infected mice exhibit increased morbidity compared with similarly treated wild-type mice

myocarditis
- CVB3-infected mice exhibit an increase in T cell infiltration in the heart compared with similarly treated wild-type mice

cardiovascular system phenotype

abnormal impulse conducting system conduction
- on days 3 and 9, CVB3-infected mice exhibit decreased E wave compared with similarly treated wild-type mice

abnormal induced retinal neovascularization
- mice exhibit 45% less ischemia-induced retinal neovascularization compared with similarly treated wild-type mice

abnormal myocardial fiber physiology
- myocytolysis is increased in CVB3-infected mice compared to in similarly treated wild-type mice

abnormal vascular smooth muscle physiology
- isolated aortic smooth muscle cells show decreased migration and capacity to contract collagen in vitro

abnormal vascular wound healing
- exhibit attenuated arterial remodeling in response to vascular injury (ligation of carotid artery) compared to wild-type, with decreases in late lumen loss, neointimal thickening, and migration of smooth muscle cells into the neointima and an accumulation of interstitial collagen of interstitial collagen

aortic aneurysm
- following induction of aortic aneurysm with elastase, mice develop fewer aneurysms with less of an increase in aortic diameter compared with similarly treated wild-type mice
- however, mice reconstituted with wild-type bone marrow exhibit normal susceptibility to elastase-induced aortic aneurysms

cardiac fibrosis
- in CVB3-infected mice compared to in similarly treated wild-type mice

decreased cardiac muscle contractility
- on day 9 post-infection in CVB3-infected mice compared to in similarly treated wild-type mice

increased susceptibility to dystrophic cardiac calcinosis
- in CVB3-infected mice compared to in similarly treated wild-type mice

myocarditis
- CVB3-infected mice exhibit an increase in T cell infiltration in the heart compared with similarly treated wild-type mice

thick interventricular septum
- CVB3-infected mice exhibit increased interventricular septum thickness compared with similarly treated wild-type mice

thick ventricular wall
- CVB3-infected mice exhibit increased left ventricular posterior wall thickness compared with similarly treated wild-type mice

nervous system phenotype

abnormal myelination
- exhibit decreased myelination in the corpus callosum at P7 and P10, but not at P14, as evidenced by decreased MBP expression

decreased oligodendrocyte number
- exhibit a decrease in the number of mature oligondendrocytes at P10, however no differences in oligodendrocyte precursor cell numbers

muscle phenotype

abnormal vascular smooth muscle physiology
- isolated aortic smooth muscle cells show decreased migration and capacity to contract collagen in vitro

decreased cardiac muscle contractility
- on day 9 post-infection in CVB3-infected mice compared to in similarly treated wild-type mice

hematopoietic system phenotype

decreased IgE level
- mice sensitized and exposed to ovalbumin exhibit impaired ovalbumin-IgE production compared with similarly treated wild-type mice

decreased dendritic cell number
- following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice

vision/eye phenotype

abnormal induced retinal neovascularization
- mice exhibit 45% less ischemia-induced retinal neovascularization compared with similarly treated wild-type mice

References

Coussens LM; Tinkle CL; Hanahan D; Werb Z. 2000. MMP-9 supplied by bone marrow-derived cells contributes to skin carcinogenesis. In: . . MGI: J:65699

Additional - Mmp9^tm1Tvu related

Acuff HB; Carter KJ; Fingleton B; Gorden DL; Matrisian LM. 2006. Matrix metalloproteinase-9 from bone marrow-derived cells contributes to survival but not growth of tumor cells in the lung microenvironment.. In: . . MGI: J:105098
Ahn GO; Brown JM. 2008. Matrix metalloproteinase-9 is required for tumor vasculogenesis but not for angiogenesis: role of bone marrow-derived myelomonocytic cells.. In: . . MGI: J:132946
Allport JR; Lim YC; Shipley JM; Senior RM; Shapiro SD; Matsuyoshi N; Vestweber D; Luscinskas FW. 2002. Neutrophils from MMP-9- or neutrophil elastase-deficient mice show no defect in transendothelial migration under flow in vitro.. In: . . MGI: J:76606
Alvarez JI; Teale JM. 2007. Evidence for differential changes of junctional complex proteins in murine neurocysticercosis dependent upon CNS vasculature.. In: . . MGI: J:145255
Andrews KL; Betsuyaku T; Rogers S; Shipley JM; Senior RM; Miner JH. 2000. Gelatinase B (MMP-9) is not essential in the normal kidney and does not influence progression of renal disease in a mouse model of alport syndrome. In: . . MGI: J:63137
Arnould C; Lelievre-Pegorier M; Ronco P; Lelongt B. 2009. MMP9 limits apoptosis and stimulates branching morphogenesis during kidney development.. In: . . MGI: J:166319
Asahi M; Asahi K; Jung JC; del Zoppo GJ; Fini ME; Lo EH. 2000. Role for matrix metalloproteinase 9 after focal cerebral ischemia: effects of gene knockout and enzyme inhibition with BB-94.. In: . . MGI: J:79535
Asahi M; Wang X; Mori T; Sumii T; Jung JC; Moskowitz MA; Fini ME; Lo EH. 2001. Effects of matrix metalloproteinase-9 gene knock-out on the proteolysis of blood-brain barrier and white matter components after cerebral ischemia.. In: . . MGI: J:71686
Awla D; Abdulla A; Syk I; Jeppsson B; Regner S; Thorlacius H. 2012. Neutrophil-derived matrix metalloproteinase-9 is a potent activator of trypsinogen in acinar cells in acute pancreatitis.. In: . . MGI: J:183726
Bajor M; Michaluk P; Gulyassy P; Kekesi AK; Juhasz G; Kaczmarek L. 2012. Synaptic cell adhesion molecule-2 and collapsin response mediator protein-2 are novel members of the matrix metalloproteinase-9 degradome.. In: . . MGI: J:187509
Baluk P; Raymond WW; Ator E; Coussens LM; McDonald DM; Caughey GH. 2004. Matrix metalloproteinase-2 and -9 expression increases in Mycoplasma-infected airways but is not required for microvascular remodeling.. In: . . MGI: J:108152
Barnett JM; McCollum GW; Fowler JA; Duan JJ; Kay JD; Liu RQ; Bingaman DP; Penn JS. 2007. Pharmacologic and genetic manipulation of MMP-2 and -9 affects retinal neovascularization in rodent models of OIR.. In: . . MGI: J:123262
Bengatta S; Arnould C; Letavernier E; Monge M; de Preneuf HM; Werb Z; Ronco P; Lelongt B. 2009. MMP9 and SCF protect from apoptosis in acute kidney injury.. In: . . MGI: J:164043
Benson HL; Mobashery S; Chang M; Kheradmand F; Hong JS; Smith GN; Shilling RA; Wilkes DS. 2011. Endogenous matrix metalloproteinases 2 and 9 regulate activation of CD4+ and CD8+ T cells.. In: . . MGI: J:185032
Bergers G; Brekken R; McMahon G; Vu TH; Itoh T; Tamaki K; Tanzawa K; Thorpe P; Itohara S; Werb Z; Hanahan D. 2000. Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis. In: . . MGI: J:65019
Betsuyaku T; Fukuda Y; Parks WC; Shipley JM; Senior RM. 2000. Gelatinase B is required for alveolar bronchiolization after intratracheal bleomycin.. In: . . MGI: J:108171
Bonig H; Priestley GV; Oehler V; Papayannopoulou T. 2007. Hematopoietic progenitor cells (HPC) from mobilized peripheral blood display enhanced migration and marrow homing compared to steady-state bone marrow HPC.. In: . . MGI: J:123189
Bottcher T; Spreer A; Azeh I; Nau R; Gerber J. 2003. Matrix metalloproteinase-9 deficiency impairs host defense mechanisms against Streptococcus pneumoniae in a mouse model of bacterial meningitis.. In: . . MGI: J:126519
Bradley LM; Douglass MF; Chatterjee D; Akira S; Baaten BJ. 2012. Matrix metalloprotease 9 mediates neutrophil migration into the airways in response to influenza virus-induced toll-like receptor signaling.. In: . . MGI: J:195392
Brass DM; Hollingsworth JW; Cinque M; Li Z; Potts E; Toloza E; Foster WM; Schwartz DA. 2008. Chronic LPS inhalation causes emphysema-like changes in mouse lung that are associated with apoptosis.. In: . . MGI: J:154269
Bruni-Cardoso A; Johnson LC; Vessella RL; Peterson TE; Lynch CC. 2010. Osteoclast-derived matrix metalloproteinase-9 directly affects angiogenesis in the prostate tumor-bone microenvironment.. In: . . MGI: J:205237
Budatha M; Roshanravan S; Zheng Q; Weislander C; Chapman SL; Davis EC; Starcher B; Word RA; Yanagisawa H. 2011. Extracellular matrix proteases contribute to progression of pelvic organ prolapse in mice and humans.. In: . . MGI: J:173933
Cackowski FC; Anderson JL; Patrene KD; Choksi RJ; Shapiro SD; Windle JJ; Blair HC; Roodman GD. 2010. Osteoclasts are important for bone angiogenesis.. In: . . MGI: J:156315
Camp TM; Tyagi SC; Senior RM; Hayden MR; Tyagi SC. 2003. Gelatinase B(MMP-9) an apoptotic factor in diabetic transgenic mice.. In: . . MGI: J:86293
Carmeliet P; Moons L; Lijnen R; Baes M; Lemaitre V; Tipping P; Drew A; Eeckhout Y; Shapiro S; Lupu F; Collen D. 1997. Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation.. In: . . MGI: J:44387
Castaneda FE; Walia B; Vijay-Kumar M; Patel NR; Roser S; Kolachala VL; Rojas M; Wang L; Oprea G; Garg P; Gewirtz AT; Roman J; Merlin D; Sitaraman SV. 2005. Targeted deletion of metalloproteinase 9 attenuates experimental colitis in mice: central role of epithelial-derived MMP.. In: . . MGI: J:104644
Cataldo DD; Tournoy KG; Vermaelen K; Munaut C; Foidart JM; Louis R; Noel A; Pauwels RA. 2002. Matrix metalloproteinase-9 deficiency impairs cellular infiltration and bronchial hyperresponsiveness during allergen-induced airway inflammation.. In: . . MGI: J:113541
Chattopadhyay S; Shubayev VI. 2009. MMP-9 controls Schwann cell proliferation and phenotypic remodeling via IGF-1 and ErbB receptor-mediated activation of MEK/ERK pathway.. In: . . MGI: J:156203
Chetty A; Cao GJ; Severgnini M; Simon A; Warburton R; Nielsen HC. 2008. Role of matrix metalloprotease-9 in hyperoxic injury in developing lung.. In: . . MGI: J:141981
Cheung C; Marchant D; Walker EK; Luo Z; Zhang J; Yanagawa B; Rahmani M; Cox J; Overall C; Senior RM; Luo H; McManus BM. 2008. Ablation of matrix metalloproteinase-9 increases severity of viral myocarditis in mice.. In: . . MGI: J:148442
Chiao YA; Ramirez TA; Zamilpa R; Okoronkwo SM; Dai Q; Zhang J; Jin YF; Lindsey ML. 2012. Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice.. In: . . MGI: J:210077
Chintala SK; Zhang X; Austin JS; Fini ME. 2002. Deficiency in matrix metalloproteinase gelatinase B (MMP-9) protects against retinal ganglion cell death after optic nerve ligation.. In: . . MGI: J:129161
Cho A; Reidy MA. 2002. Matrix metalloproteinase-9 is necessary for the regulation of smooth muscle cell replication and migration after arterial injury.. In: . . MGI: J:109007
Choi ET; Collins ET; Marine LA; Uberti MG; Uchida H; Leidenfrost JE; Khan MF; Boc KP; Abendschein DR; Parks WC. 2005. Matrix metalloproteinase-9 modulation by resident arterial cells is responsible for injury-induced accelerated atherosclerotic plaque development in apolipoprotein E-deficient mice.. In: . . MGI: J:110044
Chun TH; Hotary KB; Sabeh F; Saltiel AR; Allen ED; Weiss SJ. 2006. A pericellular collagenase directs the 3-dimensional development of white adipose tissue.. In: . . MGI: J:115867
Chun TH; Sabeh F; Ota I; Murphy H; McDonagh KT; Holmbeck K; Birkedal-Hansen H; Allen ED; Weiss SJ. 2004. MT1-MMP-dependent neovessel formation within the confines of the three-dimensional extracellular matrix.. In: . . MGI: J:94371
Colnot C; Thompson Z; Miclau T; Werb Z; Helms JA. 2003. Altered fracture repair in the absence of MMP9.. In: . . MGI: J:91527
Copin JC; Bengualid DJ; Da Silva RF; Kargiotis O; Schaller K; Gasche Y. 2011. Recombinant tissue plasminogen activator induces blood-brain barrier breakdown by a matrix metalloproteinase-9-independent pathway after transient focal cerebral ischemia in mouse.. In: . . MGI: J:178013
Copin JC; Gasche Y. 2007. Matrix metalloproteinase-9 deficiency has no effect on glial scar formation after transient focal cerebral ischemia in mouse.. In: . . MGI: J:122495
Corry DB; Kiss A; Song LZ; Song L; Xu J; Lee SH; Werb Z; Kheradmand F. 2004. Overlapping and independent contributions of MMP2 and MMP9 to lung allergic inflammatory cell egression through decreased CC chemokines.. In: . . MGI: J:118113
Costanzo RM; Perrino LA. 2008. Peak in matrix metaloproteinases-2 levels observed during recovery from olfactory nerve injury.. In: . . MGI: J:133918
Dahiya S; Bhatnagar S; Hindi SM; Jiang C; Paul PK; Kuang S; Kumar A. 2011. Elevated levels of active matrix metalloproteinase-9 cause hypertrophy in skeletal muscle of normal and dystrophin-deficient mdx mice.. In: . . MGI: J:176891
Dahiya S; Givvimani S; Bhatnagar S; Qipshidze N; Tyagi SC; Kumar A. 2011. Osteopontin-stimulated expression of matrix metalloproteinase-9 causes cardiomyopathy in the mdx model of Duchenne muscular dystrophy.. In: . . MGI: J:179125
DeLeon-Pennell KY; de Castro Bras LE; Iyer RP; Bratton DR; Jin YF; Ripplinger CM; Lindsey ML. 2014. P. gingivalis lipopolysaccharide intensifies inflammation post-myocardial infarction through matrix metalloproteinase-9.. In: . . MGI: J:225782
Delgado-Olguin P; Dang LT; He D; Thomas S; Chi L; Sukonnik T; Khyzha N; Dobenecker MW; Fish JE; Bruneau BG. 2014. Ezh2-mediated repression of a transcriptional pathway upstream of Mmp9 maintains integrity of the developing vasculature.. In: . . MGI: J:217601
Deng J; Zhang J; Feng C; Xiong L; Zuo Z. 2014. Critical role of matrix metalloprotease-9 in chronic high fat diet-induced cerebral vascular remodelling and increase of ischaemic brain injury in micedagger.. In: . . MGI: J:230092
Deshmukh HS; Shaver C; Case LM; Dietsch M; Wesselkamper SC; Hardie WD; Korfhagen TR; Corradi M; Nadel JA; Borchers MT; Leikauf GD. 2008. Acrolein-activated matrix metalloproteinase 9 contributes to persistent mucin production.. In: . . MGI: J:149725
Dhahri D; Sato-Kusubata K; Ohki-Koizumi M; Nishida C; Tashiro Y; Munakata S; Shimazu H; Salama Y; Eiamboonsert S; Nakauchi H; Hattori K; Heissig B. 2016. Fibrinolytic crosstalk with endothelial cells expands murine mesenchymal stromal cells.. In: . . MGI: J:236265
Du R; Lu KV; Petritsch C; Liu P; Ganss R; Passegue E; Song H; Vandenberg S; Johnson RS; Werb Z; Bergers G. 2008. HIF1alpha induces the recruitment of bone marrow-derived vascular modulatory cells to regulate tumor angiogenesis and invasion.. In: . . MGI: J:132945
Ducharme A; Frantz S; Aikawa M; Rabkin E; Lindsey M; Rohde LE; Schoen FJ; Kelly RA; Werb Z; Libby P; Lee RT. 2000. Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction.. In: . . MGI: J:68211
Filippov S; Koenig GC; Chun TH; Hotary KB; Ota I; Bugge TH; Roberts JD; Fay WP; Birkedal-Hansen H; Holmbeck K; Sabeh F; Allen ED; Weiss SJ. 2005. MT1-matrix metalloproteinase directs arterial wall invasion and neointima formation by vascular smooth muscle cells.. In: . . MGI: J:100717
Fleetwood AJ; Achuthan A; Schultz H; Nansen A; Almholt K; Usher P; Hamilton JA. 2014. Urokinase plasminogen activator is a central regulator of macrophage three-dimensional invasion, matrix degradation, and adhesion.. In: . . MGI: J:210232
Galis ZS; Johnson C; Godin D; Magid R; Shipley JM; Senior RM; Ivan E. 2002. Targeted disruption of the matrix metalloproteinase-9 gene impairs smooth muscle cell migration and geometrical arterial remodeling.. In: . . MGI: J:109006
Garg P; Ravi A; Patel NR; Roman J; Gewirtz AT; Merlin D; Sitaraman SV. 2007. Matrix metalloproteinase-9 regulates MUC-2 expression through its effect on goblet cell differentiation.. In: . . MGI: J:128322
Garg P; Sarma D; Jeppsson S; Patel NR; Gewirtz AT; Merlin D; Sitaraman SV. 2010. Matrix metalloproteinase-9 functions as a tumor suppressor in colitis-associated cancer.. In: . . MGI: J:156749
Gidday JM; Gasche YG; Copin JC; Shah AR; Perez RS; Shapiro SD; Chan PH; Park TS. 2005. Leukocyte-derived matrix metalloproteinase-9 mediates blood-brain barrier breakdown and is proinflammatory after transient focal cerebral ischemia.. In: . . MGI: J:100320
Gieling RG; Wallace K; Han YP. 2009. Interleukin-1 participates in the progression from liver injury to fibrosis.. In: . . MGI: J:149597
Giraudo E; Inoue M; Hanahan D. 2004. An amino-bisphosphonate targets MMP-9-expressing macrophages and angiogenesis to impair cervical carcinogenesis.. In: . . MGI: J:92599
Givvimani S; Munjal C; Narayanan N; Aqil F; Tyagi G; Metreveli N; Tyagi SC. 2012. Hyperhomocysteinemia decreases intestinal motility leading to constipation.. In: . . MGI: J:191361
Gkogkas CG; Khoutorsky A; Cao R; Jafarnejad SM; Prager-Khoutorsky M; Giannakas N; Kaminari A; Fragkouli A; Nader K; Price TJ; Konicek BW; Graff JR; Tzinia AK; Lacaille JC; Sonenberg N. 2014. Pharmacogenetic inhibition of eIF4E-dependent Mmp9 mRNA translation reverses fragile X syndrome-like phenotypes.. In: . . MGI: J:222188
Gong Y; Hart E; Shchurin A; Hoover-Plow J. 2008. Inflammatory macrophage migration requires MMP-9 activation by plasminogen in mice.. In: . . MGI: J:140977
Greenlee KJ; Corry DB; Engler DA; Matsunami RK; Tessier P; Cook RG; Werb Z; Kheradmand F. 2006. Proteomic identification of in vivo substrates for matrix metalloproteinases 2 and 9 reveals a mechanism for resolution of inflammation.. In: . . MGI: J:140613
Gursoy-Ozdemir Y; Qiu J; Matsuoka N; Bolay H; Bermpohl D; Jin H; Wang X; Rosenberg GA; Lo EH; Moskowitz MA. 2004. Cortical spreading depression activates and upregulates MMP-9.. In: . . MGI: J:121203
Gustafsson E; Aszodi A; Ortega N; Hunziker EB; Denker HW; Werb Z; Fassler R. 2003. Role of collagen type II and perlecan in skeletal development.. In: . . MGI: J:84739
Gutierrez-Fernandez A; Inada M; Balbin M; Fueyo A; Pitiot AS; Astudillo A; Hirose K; Hirata M; Shapiro SD; Noel A; Werb Z; Krane SM; Lopez-Otin C; Puente XS. 2007. Increased inflammation delays wound healing in mice deficient in collagenase-2 (MMP-8).. In: . . MGI: J:134846
Hamada T; Duarte S; Tsuchihashi S; Busuttil RW; Coito AJ. 2009. Inducible nitric oxide synthase deficiency impairs matrix metalloproteinase-9 activity and disrupts leukocyte migration in hepatic ischemia/reperfusion injury.. In: . . MGI: J:148923
Hamano Y; Zeisberg M; Sugimoto H; Lively JC; Maeshima Y; Yang C; Hynes RO; Werb Z; Sudhakar A; Kalluri R. 2003. Physiological levels of tumstatin, a fragment of collagen IV alpha3 chain, are generated by MMP-9 proteolysis and suppress angiogenesis via alphaV beta3 integrin.. In: . . MGI: J:120382
Hangai M; Kitaya N; Xu J; Chan CK; Kim JJ; Werb Z; Ryan SJ; Brooks PC. 2002. Matrix metalloproteinase-9-dependent exposure of a cryptic migratory control site in collagen is required before retinal angiogenesis.. In: . . MGI: J:113620
Hansen CN; Fisher LC; Deibert RJ; Jakeman LB; Zhang H; Noble-Haeusslein L; White S; Basso DM. 2013. Elevated MMP-9 in the lumbar cord early after thoracic spinal cord injury impedes motor relearning in mice.. In: . . MGI: J:200751
Harijith A; Choo-Wing R; Cataltepe S; Yasumatsu R; Aghai ZH; Janer J; Andersson S; Homer RJ; Bhandari V. 2011. A role for matrix metalloproteinase 9 in IFNgamma-mediated injury in developing lungs: relevance to bronchopulmonary dysplasia.. In: . . MGI: J:214716
Hathaway CK; Grant R; Hagaman JR; Hiller S; Li F; Xu L; Chang AS; Madden VJ; Bagnell CR; Rojas M; Kim HS; Wu B; Zhou B; Smithies O; Kakoki M. 2015. Endothelin-1 critically influences cardiac function via superoxide-MMP9 cascade.. In: . . MGI: J:220962
Hattori N; Mochizuki S; Kishi K; Nakajima T; Takaishi H; D'Armiento J; Okada Y. 2009. MMP-13 plays a role in keratinocyte migration, angiogenesis, and contraction in mouse skin wound healing.. In: . . MGI: J:150790
He BJ; Joiner ML; Singh MV; Luczak ED; Swaminathan PD; Koval OM; Kutschke W; Allamargot C; Yang J; Guan X; Zimmerman K; Grumbach IM; Weiss RM; Spitz DR; Sigmund CD; Blankesteijn WM; Heymans S; Mohler PJ; Anderson ME. 2011. Oxidation of CaMKII determines the cardiotoxic effects of aldosterone.. In: . . MGI: J:180205
Heilpern AJ; Wertheim W; He J; Perides G; Bronson RT; Hu LT. 2009. Matrix metalloproteinase 9 plays a key role in lyme arthritis but not in dissemination of Borrelia burgdorferi.. In: . . MGI: J:150311
Heissig B; Hattori K; Dias S; Friedrich M; Ferris B; Hackett NR; Crystal RG; Besmer P; Lyden D; Moore MA; Werb Z; Rafii S. 2002. Recruitment of stem and progenitor cells from the bone marrow niche requires MMP-9 mediated release of kit-ligand.. In: . . MGI: J:149957
Heissig B; Lund LR; Akiyama H; Ohki M; Morita Y; Romer J; Nakauchi H; Okumura K; Ogawa H; Werb Z; Dano K; Hattori K. 2007. The plasminogen fibrinolytic pathway is required for hematopoietic regeneration.. In: . . MGI: J:149807
Heymans S; Lupu F; Terclavers S; Vanwetswinkel B; Herbert JM; Baker A; Collen D; Carmeliet P; Moons L. 2005. Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice.. In: . . MGI: J:95236
Heymans S; Luttun A; Nuyens D; Theilmeier G; Creemers E; Moons L; Dyspersin GD; Cleutjens JP; Shipley M; Angellilo A; Levi M; Nube O; Baker A; Keshet E; Lupu F; Herbert JM; Smits JF; Shapiro SD; Baes M; Borgers M; Collen D; Daemen MJ; Carmeliet P. 1999. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure.. In: . . MGI: J:124004
Hindi SM; Shin J; Ogura Y; Li H; Kumar A. 2013. Matrix metalloproteinase-9 inhibition improves proliferation and engraftment of myogenic cells in dystrophic muscle of mdx mice.. In: . . MGI: J:225186
Hirahashi J; Mekala D; Van Ziffle J; Xiao L; Saffaripour S; Wagner DD; Shapiro SD; Lowell C; Mayadas TN. 2006. Mac-1 signaling via Src-family and Syk kinases results in elastase-dependent thrombohemorrhagic vasculopathy.. In: . . MGI: J:113463
Hong JS; Greenlee KJ; Pitchumani R; Lee SH; Song LZ; Shan M; Chang SH; Park PW; Dong C; Werb Z; Bidani A; Corry DB; Kheradmand F. 2011. Dual Protective Mechanisms of Matrix Metalloproteinases 2 and 9 in Immune Defense against Streptococcus pneumoniae.. In: . . MGI: J:173212
Hsu JY; Bourguignon LY; Adams CM; Peyrollier K; Zhang H; Fandel T; Cun CL; Werb Z; Noble-Haeusslein LJ. 2008. Matrix metalloproteinase-9 facilitates glial scar formation in the injured spinal cord.. In: . . MGI: J:143052
Huang PH; Chen YH; Wang CH; Chen JS; Tsai HY; Lin FY; Lo WY; Wu TC; Sata M; Chen JW; Lin SJ. 2009. Matrix metalloproteinase-9 is essential for ischemia-induced neovascularization by modulating bone marrow-derived endothelial progenitor cells.. In: . . MGI: J:167815
Huet E; Vallee B; Delbe J; Mourah S; Pruliere-Escabasse V; Tremouilleres M; Kadomatsu K; Doan S; Baudouin C; Menashi S; Gabison EE. 2011. EMMPRIN modulates epithelial barrier function through a MMP-mediated occludin cleavage: implications in dry eye disease.. In: . . MGI: J:176312
Ichiyasu H; McCormack JM; McCarthy KM; Dombkowski D; Preffer FI; Schneeberger EE. 2004. Matrix metalloproteinase-9-deficient dendritic cells have impaired migration through tracheal epithelial tight junctions.. In: . . MGI: J:99679
Ikonomidis JS; Barbour JR; Amani Z; Stroud RE; Herron AR; McClister DM Jr; Camens SE; Lindsey ML; Mukherjee R; Spinale FG. 2005. Effects of deletion of the matrix metalloproteinase 9 gene on development of murine thoracic aortic aneurysms.. In: . . MGI: J:116808
Ilkovitch D; Lopez DM. 2009. Urokinase-mediated recruitment of myeloid-derived suppressor cells and their suppressive mechanisms are blocked by MUC1/sec.. In: . . MGI: J:148729
Ishihara M; Nishida C; Tashiro Y; Gritli I; Rosenkvist J; Koizumi M; Okaji Y; Yamamoto R; Yagita H; Okumura K; Nishikori M; Wanaka K; Tsuda Y; Okada Y; Nakauchi H; Heissig B; Hattori K. 2012. Plasmin inhibitor reduces T-cell lymphoid tumor growth by suppressing matrix metalloproteinase-9-dependent CD11b(+)/F4/80(+) myeloid cell recruitment.. In: . . MGI: J:181056
Jin DK; Shido K; Kopp HG; Petit I; Shmelkov SV; Young LM; Hooper AT; Amano H; Avecilla ST; Heissig B; Hattori K; Zhang F; Hicklin DJ; Wu Y; Zhu Z; Dunn A; Salari H; Werb Z; Hackett NR; Crystal RG; Lyden D; Rafii S. 2006. Cytokine-mediated deployment of SDF-1 induces revascularization through recruitment of CXCR4+ hemangiocytes.. In: . . MGI: J:109523
Jodele S; Chantrain CF; Blavier L; Lutzko C; Crooks GM; Shimada H; Coussens LM; Declerck YA. 2005. The contribution of bone marrow-derived cells to the tumor vasculature in neuroblastoma is matrix metalloproteinase-9 dependent.. In: . . MGI: J:97827
Johnson C; Galis ZS. 2004. Matrix metalloproteinase-2 and -9 differentially regulate smooth muscle cell migration and cell-mediated collagen organization.. In: . . MGI: J:101783
Johnson C; Sung HJ; Lessner SM; Fini ME; Galis ZS. 2004. Matrix metalloproteinase-9 is required for adequate angiogenic revascularization of ischemic tissues: potential role in capillary branching.. In: . . MGI: J:95880
Jujo K; Hamada H; Iwakura A; Thorne T; Sekiguchi H; Clarke T; Ito A; Misener S; Tanaka T; Klyachko E; Kobayashi K; Tongers J; Roncalli J; Tsurumi Y; Hagiwara N; Losordo DW. 2010. CXCR4 blockade augments bone marrow progenitor cell recruitment to the neovasculature and reduces mortality after myocardial infarction.. In: . . MGI: J:161275
Kang L; Mayes WH; James FD; Bracy DP; Wasserman DH. 2014. Matrix metalloproteinase 9 opposes diet-induced muscle insulin resistance in mice.. In: . . MGI: J:208028
Kaplan A; Spiller KJ; Towne C; Kanning KC; Choe GT; Geber A; Akay T; Aebischer P; Henderson CE. 2014. Neuronal matrix metalloproteinase-9 is a determinant of selective neurodegeneration.. In: . . MGI: J:213012
Kauppinen TM; Swanson RA. 2005. Poly(ADP-ribose) polymerase-1 promotes microglial activation, proliferation, and matrix metalloproteinase-9-mediated neuron death.. In: . . MGI: J:96548
Kaviratne M; Hesse M; Leusink M; Cheever AW; Davies SJ; McKerrow JH; Wakefield LM; Letterio JJ; Wynn TA. 2004. IL-13 activates a mechanism of tissue fibrosis that is completely TGF-beta independent.. In: . . MGI: J:92753
Kawasaki Y; Xu ZZ; Wang X; Park JY; Zhuang ZY; Tan PH; Gao YJ; Roy K; Corfas G; Lo EH; Ji RR. 2008. Distinct roles of matrix metalloproteases in the early- and late-phase development of neuropathic pain.. In: . . MGI: J:133660
Kelly EA; Tremblay ME; Gahmberg CG; Tian L; Majewska AK. 2014. Subcellular localization of intercellular adhesion molecule-5 (telencephalin) in the visual cortex is not developmentally regulated in the absence of matrix metalloproteinase-9.. In: . . MGI: J:206630
Kenny HA; Kaur S; Coussens LM; Lengyel E. 2008. The initial steps of ovarian cancer cell metastasis are mediated by MMP-2 cleavage of vitronectin and fibronectin.. In: . . MGI: J:135977
Kiaei M; Kipiani K; Calingasan NY; Wille E; Chen J; Heissig B; Rafii S; Lorenzl S; Beal MF. 2007. Matrix metalloproteinase-9 regulates TNF-alpha and FasL expression in neuronal, glial cells and its absence extends life in a transgenic mouse model of amyotrophic lateral sclerosis.. In: . . MGI: J:141587
Kim Y; Remacle AG; Chernov AV; Liu H; Shubayev I; Lai C; Dolkas J; Shiryaev SA; Golubkov VS; Mizisin AP; Strongin AY; Shubayev VI. 2012. The MMP-9/TIMP-1 axis controls the status of differentiation and function of myelin-forming Schwann cells in nerve regeneration.. In: . . MGI: J:187041
Kluger MA; Zahner G; Paust HJ; Schaper M; Magnus T; Panzer U; Stahl RA. 2013. Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis.. In: . . MGI: J:202441
Kobayashi H; Chattopadhyay S; Kato K; Dolkas J; Kikuchi S; Myers RR; Shubayev VI. 2008. MMPs initiate Schwann cell-mediated MBP degradation and mechanical nociception after nerve damage.. In: . . MGI: J:143357
Kobayashi T; Kim H; Liu X; Sugiura H; Kohyama T; Fang Q; Wen FQ; Abe S; Wang X; Atkinson JJ; Shipley JM; Senior RM; Rennard SI. 2014. Matrix metalloproteinase-9 activates TGF-beta and stimulates fibroblast contraction of collagen gels.. In: . . MGI: J:221755
Koenig GC; Rowe RG; Day SM; Sabeh F; Atkinson JJ; Cooke KR; Weiss SJ. 2012. MT1-MMP-Dependent Remodeling of Cardiac Extracellular Matrix Structure and Function Following Myocardial Infarction.. In: . . MGI: J:183626
Korol A; Pino G; Dwivedi D; Robertson JV; Deschamps PA; West-Mays JA. 2014. Matrix Metalloproteinase-9-Null Mice Are Resistant to TGF-beta-Induced Anterior Subcapsular Cataract Formation.. In: . . MGI: J:211036
Kowluru RA; Mohammad G; dos Santos JM; Zhong Q. 2011. Abrogation of MMP-9 gene protects against the development of retinopathy in diabetic mice by preventing mitochondrial damage.. In: . . MGI: J:189477
Kubota Y; Takubo K; Shimizu T; Ohno H; Kishi K; Shibuya M; Saya H; Suda T. 2009. M-CSF inhibition selectively targets pathological angiogenesis and lymphangiogenesis.. In: . . MGI: J:148497
Kurihara T; Shimizu-Hirota R; Shimoda M; Adachi T; Shimizu H; Weiss SJ; Itoh H; Hori S; Aikawa N; Okada Y. 2012. Neutrophil-derived matrix metalloproteinase 9 triggers acute aortic dissection.. In: . . MGI: J:210144
Kyriakides TR; Wulsin D; Skokos EA; Fleckman P; Pirrone A; Shipley JM; Senior RM; Bornstein P. 2009. Mice that lack matrix metalloproteinase-9 display delayed wound healing associated with delayed reepithelization and disordered collagen fibrillogenesis.. In: . . MGI: J:149139
Lambert V; Wielockx B; Munaut C; Galopin C; Jost M; Itoh T; Werb Z; Baker A; Libert C; Krell HW; Foidart JM; Noel A; Rakic JM. 2003. MMP-2 and MMP-9 synergize in promoting choroidal neovascularization.. In: . . MGI: J:86805
Lanone S; Zheng T; Zhu Z; Liu W; Lee CG; Ma B; Chen Q; Homer RJ; Wang J; Rabach LA; Rabach ME; Shipley JM; Shapiro SD; Senior RM; Elias JA. 2002. Overlapping and enzyme-specific contributions of matrix metalloproteinases-9 and -12 in IL-13-induced inflammation and remodeling.. In: . . MGI: J:78575
Larsen PH; DaSilva AG; Conant K; Yong VW. 2006. Myelin formation during development of the CNS is delayed in matrix metalloproteinase-9 and -12 null mice.. In: . . MGI: J:105765
Larsen PH; Wells JE; Stallcup WB; Opdenakker G; Yong VW. 2003. Matrix metalloproteinase-9 facilitates remyelination in part by processing the inhibitory NG2 proteoglycan.. In: . . MGI: J:87968
Lee CG; Homer RJ; Zhu Z; Lanone S; Wang X; Koteliansky V; Shipley JM; Gotwals P; Noble P; Chen Q; Senior RM; Elias JA. 2001. Interleukin-13 induces tissue fibrosis by selectively stimulating and activating transforming growth factor beta(1).. In: . . MGI: J:119457
Lee MM; Yoon BJ; Osiewicz K; Preston M; Bundy B; van Heeckeren AM; Werb Z; Soloway PD. 2005. Tissue inhibitor of metalloproteinase 1 regulates resistance to infection.. In: . . MGI: J:94836
Lee SR; Tsuji K; Lee SR; Lo EH. 2004. Role of matrix metalloproteinases in delayed neuronal damage after transient global cerebral ischemia.. In: . . MGI: J:87728
Lee SY; Horbelt M; Mang HE; Knipe NL; Bacallao RL; Sado Y; Sutton TA. 2011. MMP-9 gene deletion mitigates microvascular loss in a model of ischemic acute kidney injury.. In: . . MGI: J:174034
Lelongt B; Bengatta S; Delauche M; Lund LR; Werb Z; Ronco PM. 2001. Matrix metalloproteinase 9 protects mice from anti-glomerular basement membrane nephritis through its fibrinolytic activity.. In: . . MGI: J:68656
Levesque JP; Liu F; Simmons PJ; Betsuyaku T; Senior RM; Pham C; Link DC. 2004. Characterization of hematopoietic progenitor mobilization in protease-deficient mice.. In: . . MGI: J:90920
Li H; Mittal A; Makonchuk DY; Bhatnagar S; Kumar A. 2009. Matrix metalloproteinase-9 inhibition ameliorates pathogenesis and improves skeletal muscle regeneration in muscular dystrophy.. In: . . MGI: J:150030
Li H; Mittal A; Paul PK; Kumar M; Srivastava DS; Tyagi SC; Kumar A. 2009. Tumor necrosis factor-related weak inducer of apoptosis augments matrix metalloproteinase 9 (MMP-9) production in skeletal muscle through the activation of nuclear factor-kappaB-inducing kinase and p38 mitogen-activated protein kinase: a potential role of MMP-9 in myopathy.. In: . . MGI: J:147593
Lian X; Qin Y; Hossain SA; Yang L; White A; Xu H; Shipley JM; Li T; Senior RM; Du H; Yan C. 2005. Overexpression of Stat3C in pulmonary epithelium protects against hyperoxic lung injury.. In: . . MGI: J:98964
Lieu S; Hansen E; Dedini R; Behonick D; Werb Z; Miclau T; Marcucio R; Colnot C. 2011. Impaired remodeling phase of fracture repair in the absence of matrix metalloproteinase-2.. In: . . MGI: J:237173
Lim DH; Cho JY; Miller M; McElwain K; McElwain S; Broide DH. 2006. Reduced peribronchial fibrosis in allergen-challenged MMP-9-deficient mice.. In: . . MGI: J:144403
Lin CH; Lee HT; Lee SD; Lee W; Cho CW; Lin SZ; Wang HJ; Okano H; Su CY; Yu YL; Hsu CY; Shyu WC. 2013. Role of HIF-1alpha-activated Epac1 on HSC-mediated neuroplasticity in stroke model.. In: . . MGI: J:201546
Lindsey ML; Escobar GP; Dobrucki LW; Goshorn DK; Bouges S; Mingoia JT; McClister DM Jr; Su H; Gannon J; MacGillivray C; Lee RT; Sinusas AJ; Spinale FG. 2006. Matrix metalloproteinase-9 gene deletion facilitates angiogenesis after myocardial infarction.. In: . . MGI: J:104786
Littlepage LE; Sternlicht MD; Rougier N; Phillips J; Gallo E; Yu Y; Williams K; Brenot A; Gordon JI; Werb Z. 2010. Matrix metalloproteinases contribute distinct roles in neuroendocrine prostate carcinogenesis, metastasis, and angiogenesis progression.. In: . . MGI: J:157977
Liu Z; Shipley JM; Vu TH; Zhou X; Diaz LA; Werb Z; Senior RM. 1998. Gelatinase B-deficient mice are resistant to experimental bullous pemphigoid.. In: . . MGI: J:91478
Liu Z; Zhou X; Shapiro SD; Shipley JM; Twining SS; Diaz LA; Senior RM; Werb Z. 2000. The serpin alpha1-proteinase inhibitor is a critical substrate for gelatinase B/MMP-9 in vivo.. In: . . MGI: J:64322
Longo GM; Xiong W; Greiner TC; Zhao Y; Fiotti N; Baxter BT. 2002. Matrix metalloproteinases 2 and 9 work in concert to produce aortic aneurysms.. In: . . MGI: J:118409
Lukkarinen H; Hogmalm A; Lappalainen U; Bry K. 2009. Matrix metalloproteinase-9 deficiency worsens lung injury in a model of bronchopulmonary dysplasia.. In: . . MGI: J:161580
Lund IK; Nielsen BS; Almholt K; Rono B; Hald A; Illemann M; Green KA; Christensen IJ; Romer J; Lund LR. 2011. Concomitant lack of MMP9 and uPA disturbs physiological tissue remodeling.. In: . . MGI: J:176606
MacLauchlan S; Skokos EA; Meznarich N; Zhu DH; Raoof S; Shipley JM; Senior RM; Bornstein P; Kyriakides TR. 2009. Macrophage fusion, giant cell formation, and the foreign body response require matrix metalloproteinase 9.. In: . . MGI: J:146904
Malik M; Bakshi CS; McCabe K; Catlett SV; Shah A; Singh R; Jackson PL; Gaggar A; Metzger DW; Melendez JA; Blalock JE; Sellati TJ. 2007. Matrix metalloproteinase 9 activity enhances host susceptibility to pulmonary infection with type A and B strains of Francisella tularensis.. In: . . MGI: J:142623
Martin MD; Carter KJ; Jean-Philippe SR; Chang M; Mobashery S; Thiolloy S; Lynch CC; Matrisian LM; Fingleton B. 2008. Effect of ablation or inhibition of stromal matrix metalloproteinase-9 on lung metastasis in a breast cancer model is dependent on genetic background.. In: . . MGI: J:140033
Masson V; de la Ballina LR; Munaut C; Wielockx B; Jost M; Maillard C; Blacher S; Bajou K; Itoh T; Itohara S; Werb Z; Libert C; Foidart JM; Noel A. 2005. Contribution of host MMP-2 and MMP-9 to promote tumor vascularization and invasion of malignant keratinocytes.. In: . . MGI: J:105100
McClellan SA; Huang X; Barrett RP; Lighvani S; Zhang Y; Richiert D; Hazlett LD. 2006. Matrix Metalloproteinase-9 Amplifies the Immune Response to Pseudomonas aeruginosa Corneal Infection.. In: . . MGI: J:104273
McMillan SJ; Kearley J; Campbell JD; Zhu XW; Larbi KY; Shipley JM; Senior RM; Nourshargh S; Lloyd CM. 2004. Matrix metalloproteinase-9 deficiency results in enhanced allergen-induced airway inflammation.. In: . . MGI: J:88065
Mohan R; Chintala SK; Jung JC; Villar WV; McCabe F; Russo LA; Lee Y; McCarthy BE; Wollenberg KR; Jester JV; Wang M; Welgus HG; Shipley JM; Senior RM; Fini ME. 2002. Matrix metalloproteinase gelatinase B (MMP-9) coordinates and effects epithelial regeneration.. In: . . MGI: J:124833
Nagy V; Bozdagi O; Matynia A; Balcerzyk M; Okulski P; Dzwonek J; Costa RM; Silva AJ; Kaczmarek L; Huntley GW. 2006. Matrix metalloproteinase-9 is required for hippocampal late-phase long-term potentiation and memory.. In: . . MGI: J:105763
Nakahara F; Kitaura J; Uchida T; Nishida C; Togami K; Inoue D; Matsukawa T; Kagiyama Y; Enomoto Y; Kawabata KC; Chen-Yi L; Komeno Y; Izawa K; Oki T; Nagae G; Harada Y; Harada H; Otsu M; Aburatani H; Heissig B; Hattori K; Kitamura T. 2014. Hes1 promotes blast crisis in chronic myelogenous leukemia through MMP-9 upregulation in leukemic cells.. In: . . MGI: J:211273
Nakasone ES; Askautrud HA; Kees T; Park JH; Plaks V; Ewald AJ; Fein M; Rasch MG; Tan YX; Qiu J; Park J; Sinha P; Bissell MJ; Frengen E; Werb Z; Egeblad M. 2012. Imaging tumor-stroma interactions during chemotherapy reveals contributions of the microenvironment to resistance.. In: . . MGI: J:189331
Nguyen KP; McGilvray KC; Puttlitz CM; Mukhopadhyay S; Chabasse C; Sarkar R. 2015. Matrix Metalloproteinase 9 (MMP-9) Regulates Vein Wall Biomechanics in Murine Thrombus Resolution.. In: . . MGI: J:243326
Nicoud IB; Jones CM; Pierce JM; Earl TM; Matrisian LM; Chari RS; Gorden DL. 2007. Warm hepatic ischemia-reperfusion promotes growth of colorectal carcinoma micrometastases in mouse liver via matrix metalloproteinase-9 induction.. In: . . MGI: J:120314
Nishikii H; Eto K; Tamura N; Hattori K; Heissig B; Kanaji T; Sawaguchi A; Goto S; Ware J; Nakauchi H. 2008. Metalloproteinase regulation improves in vitro generation of efficacious platelets from mouse embryonic stem cells.. In: . . MGI: J:138214
Noble LJ; Donovan F; Igarashi T; Goussev S; Werb Z. 2002. Matrix metalloproteinases limit functional recovery after spinal cord injury by modulation of early vascular events.. In: . . MGI: J:124001
Nuki Y; Tsou TL; Kurihara C; Kanematsu M; Kanematsu Y; Hashimoto T. 2009. Elastase-induced intracranial aneurysms in hypertensive mice.. In: . . MGI: J:177972
Ohki M; Ohki Y; Ishihara M; Nishida C; Tashiro Y; Akiyama H; Komiyama H; Lund LR; Nitta A; Yamada K; Zhu Z; Ogawa H; Yagita H; Okumura K; Nakauchi H; Werb Z; Heissig B; Hattori K. 2010. Tissue type plasminogen activator regulates myeloid-cell dependent neoangiogenesis during tissue regeneration.. In: . . MGI: J:160268
Ortega N; Behonick DJ; Colnot C; Cooper DN; Werb Z. 2005. Galectin-3 is a downstream regulator of matrix metalloproteinase-9 function during endochondral bone formation.. In: . . MGI: J:100747
Ortega N; Wang K; Ferrara N; Werb Z; Vu TH. 2010. Complementary interplay between matrix metalloproteinase-9, vascular endothelial growth factor and osteoclast function drives endochondral bone formation.. In: . . MGI: J:160852
Ovechkin AV; Tyagi N; Rodriguez WE; Hayden MR; Moshal KS; Tyagi SC. 2005. Role of matrix metalloproteinase-9 in endothelial apoptosis in chronic heart failure in mice.. In: . . MGI: J:116865
Page K; Ledford JR; Zhou P; Wills-Karp M. 2009. A TLR2 agonist in German cockroach frass activates MMP-9 release and is protective against allergic inflammation in mice.. In: . . MGI: J:151856
Paiva KB; Granjeiro JM. 2014. Bone tissue remodeling and development: focus on matrix metalloproteinase functions.. In: . . MGI: J:230211
Park SJ; Wiekowski MT; Lira SA; Mehrad B. 2006. Neutrophils regulate airway responses in a model of fungal allergic airways disease.. In: . . MGI: J:129184
Perez SE; Cano DA; Dao-Pick T; Rougier JP; Werb Z; Hebrok M. 2005. Matrix metalloproteinases 2 and 9 are dispensable for pancreatic islet formation and function in vivo.. In: . . MGI: J:105134
Pflugfelder SC; Farley W; Luo L; Chen LZ; de Paiva CS; Olmos LC; Li DQ; Fini ME. 2005. Matrix metalloproteinase-9 knockout confers resistance to corneal epithelial barrier disruption in experimental dry eye.. In: . . MGI: J:95266
Pyo R; Lee JK; Shipley JM; Curci JA; Mao D; Ziporin SJ; Ennis TL; Shapiro SD; Senior RM; Thompson RW. 2000. Targeted gene disruption of matrix metalloproteinase-9 (gelatinase B) suppresses development of experimental abdominal aortic aneurysms [see comments]. In: . . MGI: J:62760
Ratzinger G; Stoitzner P; Ebner S; Lutz MB; Layton GT; Rainer C; Senior RM; Shipley JM; Fritsch P; Schuler G; Romani N. 2002. Matrix metalloproteinases 9 and 2 are necessary for the migration of Langerhans cells and dermal dendritic cells from human and murine skin.. In: . . MGI: J:76157
Renckens R; Roelofs JJ; Florquin S; de Vos AF; Lijnen HR; van't Veer C; van der Poll T. 2006. Matrix metalloproteinase-9 deficiency impairs host defense against abdominal sepsis.. In: . . MGI: J:129550
Robertson JV; Siwakoti A; West-Mays JA. 2013. Altered expression of transforming growth factor beta 1 and matrix metalloproteinase-9 results in elevated intraocular pressure in mice.. In: . . MGI: J:196164
Sabeh F; Li XY; Saunders TL; Rowe RG; Weiss SJ. 2009. Secreted versus membrane-anchored collagenases: relative roles in fibroblast-dependent collagenolysis and invasion.. In: . . MGI: J:153449
Sahay B; Singh A; Gnanamani A; Patsey RL; Blalock JE; Sellati TJ. 2011. CD14 signaling reciprocally controls collagen deposition and turnover to regulate the development of lyme arthritis.. In: . . MGI: J:169078
Senft AP; Korfhagen TR; Whitsett JA; Shapiro SD; LeVine AM. 2005. Surfactant protein-D regulates soluble CD14 through matrix metalloproteinase-12.. In: . . MGI: J:98168
Shiba N; Miyazaki D; Yoshizawa T; Fukushima K; Shiba Y; Inaba Y; Imamura M; Takeda S; Koike K; Nakamura A. 2015. Differential roles of MMP-9 in early and late stages of dystrophic muscles in a mouse model of Duchenne muscular dystrophy.. In: . . MGI: J:231193
Shubayev VI; Angert M; Dolkas J; Campana WM; Palenscar K; Myers RR. 2006. TNFalpha-induced MMP-9 promotes macrophage recruitment into injured peripheral nerve.. In: . . MGI: J:106877
Sidhu H; Dansie LE; Hickmott PW; Ethell DW; Ethell IM. 2014. Genetic removal of matrix metalloproteinase 9 rescues the symptoms of fragile X syndrome in a mouse model.. In: . . MGI: J:215594
Stickens D; Behonick DJ; Ortega N; Heyer B; Hartenstein B; Yu Y; Fosang AJ; Schorpp-Kistner M; Angel P; Werb Z. 2004. Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.. In: . . MGI: J:94460
Stowe AM; Adair-Kirk TL; Gonzales ER; Perez RS; Shah AR; Park TS; Gidday JM. 2009. Neutrophil elastase and neurovascular injury following focal stroke and reperfusion.. In: . . MGI: J:150458
Su J; Palen DI; Lucchesi PA; Matrougui K. 2006. Mice lacking the gene encoding for MMP-9 and resistance artery reactivity.. In: . . MGI: J:113095
Sullivan BP; Kassel KM; Jone A; Flick MJ; Luyendyk JP. 2012. Fibrin(ogen)-Independent Role of Plasminogen Activators in Acetaminophen-Induced Liver Injury.. In: . . MGI: J:184692
Suofu Y; Clark JF; Broderick JP; Kurosawa Y; Wagner KR; Lu A. 2012. Matrix metalloproteinase-2 or -9 deletions protect against hemorrhagic transformation during early stage of cerebral ischemia and reperfusion.. In: . . MGI: J:184676
Suzuki Y; Nagai N; Umemura K; Collen D; Lijnen HR. 2007. Stromelysin-1 (MMP-3) is critical for intracranial bleeding after t-PA treatment of stroke in mice.. In: . . MGI: J:148570
Svedin P; Hagberg H; Savman K; Zhu C; Mallard C. 2007. Matrix metalloproteinase-9 gene knock-out protects the immature brain after cerebral hypoxia-ischemia.. In: . . MGI: J:141740
Takabayshi K; Corr M; Hayashi T; Redecke V; Beck L; Guiney D; Sheppard D; Raz E. 2006. Induction of a homeostatic circuit in lung tissue by microbial compounds.. In: . . MGI: J:113350
Taylor JL; Hattle JM; Dreitz SA; Troudt JM; Izzo LS; Basaraba RJ; Orme IM; Matrisian LM; Izzo AA. 2006. Role for Matrix Metalloproteinase 9 in Granuloma Formation during Pulmonary Mycobacterium tuberculosis Infection.. In: . . MGI: J:113558
Thiolloy S; Halpern J; Holt GE; Schwartz HS; Mundy GR; Matrisian LM; Lynch CC. 2009. Osteoclast-derived matrix metalloproteinase-7, but not matrix metalloproteinase-9, contributes to tumor-induced osteolysis.. In: . . MGI: J:151928
Tian L; Stefanidakis M; Ning L; Van Lint P; Nyman-Huttunen H; Libert C; Itohara S; Mishina M; Rauvala H; Gahmberg CG. 2007. Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage.. In: . . MGI: J:150623
Tian W; Kyriakides TR. 2009. Matrix metalloproteinase-9 deficiency leads to prolonged foreign body response in the brain associated with increased IL-1beta levels and leakage of the blood-brain barrier.. In: . . MGI: J:148956
Ulyanova T; Priestley GV; Banerjee ER; Papayannopoulou T. 2007. Unique and redundant roles of alpha4 and beta2 integrins in kinetics of recruitment of lymphoid vs myeloid cell subsets to the inflamed peritoneum revealed by studies of genetically deficient mice.. In: . . MGI: J:126483
Urbich C; Heeschen C; Aicher A; Sasaki K; Bruhl T; Farhadi MR; Vajkoczy P; Hofmann WK; Peters C; Pennacchio LA; Abolmaali ND; Chavakis E; Reinheckel T; Zeiher AM; Dimmeler S. 2005. Cathepsin L is required for endothelial progenitor cell-induced neovascularization.. In: . . MGI: J:99594
Vaillant C; Meissirel C; Mutin M; Belin MF; Lund LR; Thomasset N. 2003. MMP-9 deficiency affects axonal outgrowth, migration, and apoptosis in the developing cerebellum.. In: . . MGI: J:126201
Vanden Berghe T; Hulpiau P; Martens L; Vandenbroucke RE; Van Wonterghem E; Perry SW; Bruggeman I; Divert T; Choi SM; Vuylsteke M; Shestopalov VI; Libert C; Vandenabeele P. 2015. Passenger Mutations Confound Interpretation of All Genetically Modified Congenic Mice.. In: . . MGI: J:229106
Vermaelen KY; Cataldo D; Tournoy K; Maes T; Dhulst A; Louis R; Foidart JM; Noel A; Pauwels R. 2003. Matrix metalloproteinase-9-mediated dendritic cell recruitment into the airways is a critical step in a mouse model of asthma.. In: . . MGI: J:84293
Vu TH; Shipley JM; Bergers G; Berger JE; Helms JA; Hanahan D; Shapiro SD; Senior RM; Werb Z. 1998. MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes.. In: . . MGI: J:47297
Wang CH; Anderson N; Li SH; Szmitko PE; Cherng WJ; Fedak PW; Fazel S; Li RK; Yau TM; Weisel RD; Stanford WL; Verma S. 2006. Stem cell factor deficiency is vasculoprotective: unraveling a new therapeutic potential of imatinib mesylate.. In: . . MGI: J:125065
Wang G; Guo Q; Hossain M; Fazio V; Zeynalov E; Janigro D; Mayberg MR; Namura S. 2009. Bone marrow-derived cells are the major source of MMP-9 contributing to blood-brain barrier dysfunction and infarct formation after ischemic stroke in mice.. In: . . MGI: J:157206
Wang M; Qin X; Mudgett JS; Ferguson TA; Senior RM; Welgus HG. 1999. Matrix metalloproteinase deficiencies affect contact hypersensitivity: stromelysin-1 deficiency prevents the response and gelatinase B deficiency prolongs the response.. In: . . MGI: J:55723
Wang P; Dai J; Bai F; Kong KF; Wong SJ; Montgomery RR; Madri JA; Fikrig E. 2008. Matrix metalloproteinase 9 facilitates West Nile virus entry into the brain.. In: . . MGI: J:153406
Wang X; Jung J; Asahi M; Chwang W; Russo L; Moskowitz MA; Dixon CE; Fini ME; Lo EH. 2000. Effects of matrix metalloproteinase-9 gene knock-out on morphological and motor outcomes after traumatic brain injury.. In: . . MGI: J:79422
Wang X; Zhou Y; Tan R; Xiong M; He W; Fang L; Wen P; Jiang L; Yang J. 2010. Mice lacking the matrix metalloproteinase-9 gene reduce renal interstitial fibrosis in obstructive nephropathy.. In: . . MGI: J:165577
Warner RL; Beltran L; Younkin EM; Lewis CS; Weiss SJ; Varani J; Johnson KJ. 2001. Role of stromelysin 1 and gelatinase B in experimental acute lung injury.. In: . . MGI: J:114188
West MA; Prescott AR; Chan KM; Zhou Z; Rose-John S; Scheller J; Watts C. 2008. TLR ligand-induced podosome disassembly in dendritic cells is ADAM17 dependent.. In: . . MGI: J:138782
Xiong W; Knispel R; MacTaggart J; Greiner TC; Weiss SJ; Baxter BT. 2009. Membrane-type 1 matrix metalloproteinase regulates macrophage-dependent elastolytic activity and aneurysm formation in vivo.. In: . . MGI: J:145884
Xu B; Chen H; Xu W; Zhang W; Buckley S; Zheng SG; Warburton D; Kolb M; Gauldie J; Shi W. 2012. Molecular mechanisms of MMP9 overexpression and its role in emphysema pathogenesis of Smad3-deficient mice.. In: . . MGI: J:191358
Xu J; Mora A; Shim H; Stecenko A; Brigham KL; Rojas M. 2007. Role of the SDF-1/CXCR4 axis in the pathogenesis of lung injury and fibrosis.. In: . . MGI: J:138491
Xu J; Park PW; Kheradmand F; Corry DB. 2005. Endogenous attenuation of allergic lung inflammation by syndecan-1.. In: . . MGI: J:98401
Xue M; Hollenberg MD; Yong VW. 2006. Combination of thrombin and matrix metalloproteinase-9 exacerbates neurotoxicity in cell culture and intracerebral hemorrhage in mice.. In: . . MGI: J:112950
Yabluchanskiy A; Ma Y; Chiao YA; Lopez EF; Voorhees AP; Toba H; Hall ME; Han HC; Lindsey ML; Jin YF. 2014. Cardiac aging is initiated by matrix metalloproteinase-9-mediated endothelial dysfunction.. In: . . MGI: J:211679
Yan B; Wei JJ; Yuan Y; Sun R; Li D; Luo J; Liao SJ; Zhou YH; Shu Y; Wang Q; Zhang GM; Feng ZH. 2013. IL-6 cooperates with G-CSF to induce protumor function of neutrophils in bone marrow by enhancing STAT3 activation.. In: . . MGI: J:204780
Yen JH; Khayrullina T; Ganea D. 2008. PGE2-induced metalloproteinase-9 is essential for dendritic cell migration.. In: . . MGI: J:130104
Yepes M; Sandkvist M; Moore EG; Bugge TH; Strickland DK; Lawrence DA. 2003. Tissue-type plasminogen activator induces opening of the blood-brain barrier via the LDL receptor-related protein.. In: . . MGI: J:119309
Yin KJ; Cirrito JR; Yan P; Hu X; Xiao Q; Pan X; Bateman R; Song H; Hsu FF; Turk J; Xu J; Hsu CY; Mills JC; Holtzman DM; Lee JM. 2006. Matrix metalloproteinases expressed by astrocytes mediate extracellular amyloid-beta peptide catabolism.. In: . . MGI: J:114690
Zajac E; Schweighofer B; Kupriyanova TA; Juncker-Jensen A; Minder P; Quigley JP; Deryugina EI. 2013. Angiogenic capacity of M1- and M2-polarized macrophages is determined by the levels of TIMP-1 complexed with their secreted proMMP-9.. In: . . MGI: J:207707
Zeisberg M; Khurana M; Rao VH; Cosgrove D; Rougier JP; Werner MC; Shield CF 3rd; Werb Z; Kalluri R. 2006. Stage-specific action of matrix metalloproteinases influences progressive hereditary kidney disease.. In: . . MGI: J:134125
Zhang L; Ikegami M; Korfhagen TR; McCormack FX; Yoshida M; Senior RM; Shipley JM; Shapiro SD; Whitsett JA. 2006. Neither SP-A nor NH2-terminal domains of SP-A can substitute for SP-D in regulation of alveolar homeostasis.. In: . . MGI: J:121212
Zhong Q; Kowluru RA. 2013. Regulation of matrix metalloproteinase-9 by epigenetic modifications and the development of diabetic retinopathy.. In: . . MGI: J:208549
van Deventer HW; Palmieri DA; Wu QP; McCook EC; Serody JS. 2013. Circulating Fibrocytes Prepare the Lung for Cancer Metastasis by Recruiting Ly-6C+ Monocytes Via CCL2.. In: . . MGI: J:195511

Also Known As: MMP-9-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Mmp9tm1Tvu

Allele Symbol: Mmp9tm1Tvu

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Mmp9tm1Tvu related

Mammalian Phenotype Terms by Genotype

Genotype: Mmp9tm1Tvu/Mmp9tm1TvuB6.129S6-Mmp9tm1Tvu

neoplasm

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvueither: (involves: 129S6/SvEvTac) or (involves: 129S6/SvEvTac * C57BL/6J)

cardiovascular system phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvuinvolves: 129S6/SvEvTac * C57BL/6J

cardiovascular system phenotype

muscle phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvuinvolves: 129S6/SvEvTac * C57BL/6

immune system phenotype

homeostasis/metabolism phenotype

respiratory system phenotype

hematopoietic system phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvueither: (involves: 129S6/SvEvTac * Black Swiss) or (involves: 129S6/SvEvTac * CD-1)

skeleton phenotype

limbs/digits/tail phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvueither: FVB.129S6-Mmp9tm1Tvu or (involves: 129S6/SvEvTac)

cardiovascular system phenotype

homeostasis/metabolism phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvuinvolves: 129/Sv * 129S6/SvEvTac

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvuinvolves: 129S6/SvEvTac * FVB/N

nervous system phenotype

homeostasis/metabolism phenotype

cellular phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1TvuFVB.129S6-Mmp9tm1Tvu

mortality/aging

cardiovascular system phenotype

immune system phenotype

homeostasis/metabolism phenotype

muscle phenotype

digestive/alimentary phenotype

hematopoietic system phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1TvuC3N.129S6-Mmp9tm1Tvu

immune system phenotype

skeleton phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1TvuFVB.Cg-Mmp9tm1Tvu/J

mortality/aging

integument phenotype

immune system phenotype

digestive/alimentary phenotype

behavior/neurological phenotype

homeostasis/metabolism phenotype

cardiovascular system phenotype

nervous system phenotype

growth/size/body region phenotype

muscle phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvu129S6/SvEvTac-Mmp9tm1Tvu

immune system phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvuinvolves: 129S6/SvEvTac * C57BL/6 * C57BL/6NTac

behavior/neurological phenotype

nervous system phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvuinvolves: 129S6/SvEvTac * CD-1

mortality/aging

hematopoietic system phenotype

homeostasis/metabolism phenotype

nervous system phenotype

immune system phenotype

vision/eye phenotype

cellular phenotype

Genotype: Mmp9tm1Tvu/Mmp9tm1Tvuinvolves: 129S6/SvEvTac

mortality/aging

homeostasis/metabolism phenotype

Also Known As: MMP-9^-

Mmp9^tm1Tvu

Allele Symbol: Mmp9^tm1Tvu

Genotype: Mmp9^tm1Tvu related

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
B6.129S6-Mmp9^tm1Tvu

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
either: (involves: 129S6/SvEvTac) or (involves: 129S6/SvEvTac * C57BL/6J)

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * C57BL/6J

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * C57BL/6

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
either: (involves: 129S6/SvEvTac * Black Swiss) or (involves: 129S6/SvEvTac * CD-1)

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
either: FVB.129S6-Mmp9^tm1Tvu or (involves: 129S6/SvEvTac)

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129/Sv * 129S6/SvEvTac

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * FVB/N

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
FVB.129S6-Mmp9^tm1Tvu

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
C3N.129S6-Mmp9^tm1Tvu

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
FVB.Cg-Mmp9^tm1Tvu/J

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
129S6/SvEvTac-Mmp9^tm1Tvu

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NTac

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac * CD-1

Genotype: Mmp9^tm1Tvu/Mmp9^tm1Tvu
involves: 129S6/SvEvTac

Additional - Mmp9^tm1Tvu related