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 Cell 103(3):481-90. PubMed: 11081634 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

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Additional - Mmp9^tm1Tvu related

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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. Nat Med 11(2):206-13. PubMed: 15665831 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. Mol Cell Neurosci 24(2):395-408. PubMed: 14572461 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. Immunity 43(1):200-9. PubMed: 26163370 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. J Immunol 171(2):1016-22. PubMed: 12847275 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. Cell 93(3):411-22. PubMed: 9590175 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. Circ Res 99(6):617-25. PubMed: 16931795 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. Brain Res 1294:183-92. PubMed: 19646426 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. Proc Natl Acad Sci U S A 96(12):6885-9. PubMed: 10359808 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. J Virol 82(18):8978-85. PubMed: 18632868 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. J Neurosci 20(18):7037-42. PubMed: 10995849 MGI: J:79422
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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