JAX
Mouse Strain Datasheet - 008340
BKS.Cg-Leprdb Nos3tm1Unc/RhrsJ
- Stock No:
- 008340 |
- eNOS-/- C57BLKS/J db
Also Known As: eNOS-/- C57BLKS/J db
These double mutant mice harbor both the spontaneous Leprdb mutation and nitric oxide synthase 3, endothelial cell (Nos3 or eNOS) targeted mutation. Double homozygous eNOS-/- C57BLKS/J db/db mice (also called eNOS-/- db/db, or db/db/eNOS-/- double mutant mice) are a robust model of type II diabetic nephropathy and may be useful for studying eNOS-mediated events in the development and progression of diabetic nephropathy.
Donating Investigator
Dr. Raymond C. Harris, Vanderbilt University Med Center
Genetic overview
| Genetic Background | Generation |
|---|---|
|
N11+F9
|
Leprdb
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Spontaneous | Lepr | leptin receptor |
Nos3tm1Unc
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Targeted (Null/Knockout) | Nos3 | nitric oxide synthase 3, endothelial cell |
Research Applications
- Cardiovascular Research
- Diabetes and Obesity Research
- Endocrine Deficiency Research
- Internal/Organ Research
- Metabolism Research
- Research Tools
- Immunology, Inflammation and Autoimmunity Research
- Reproductive Biology Research
Base Price
Starting at:
| $263.00 Domestic price for female |
| $526.00 Domestic price for breeder pair |
Detailed Description
These double mutant mice harbor both the Leprdb spontaneous mutation and the Nos3 (eNOS) targeted mutation and are congenic on C57BLKS/J genetic background. Mice homozygous for both mutations (called eNOS-/- C57BLKS/J db/db, eNOS-/- db/db, or db/db/eNOS-/- double mutant mice) are viable with development of type II diabetes and diabetic nephropathy. The eNOS-/- C57BLKS/J db/db mice develop type II diabetes with significant obesity and hypertension: while both mutations are associated with insulin resistance, the mutated leptin receptor in db/db mice chiefly accounts for the observed hyperglycemia and defective leptin signaling (leading to persistent hyperphagia and obesity), and the eNOS-deficiency accounts for the moderate systemic hypertension. In addition, eNOS-/- C57BLKS/J db/db mice exhibit rapid onset and progression of pathologic diabetic nephropathy (DN) features by 26 weeks of age; developing severe albuminuria and other DN characteristics (including arteriolar hyalinosis, increased glomerular basement membrane thickness, mesangial expansion, mesangiolysis, and focal segmental and early nodular glomerulosclerosis), also with remarkably decreased glomerular filtration rate (GFR; on the basis of impaired inulin clearance and increased serum creatinine). Double homozygous eNOS-/- C57BLKS/J db/db mice are a robust model of type II diabetic nephropathy and may be useful for studying eNOS-mediated events in the development and progression of diabetic nephropathy.
Development
These eNOS- C57BLKS/J Leprdb double mutant mice were generated in the laboratory of Dr. Raymond C. Harris (Vanderbilt University) by backcrossing eNOS-mutant mice (Stock No. 002684) to C57BLKS/J inbred mice (Stock No. 000662) for 10 generations, and then the resulting mice were bred with the BKS.Cg-Dock7m +/+ Leprdb/J repulsion stock (Stock No. 000642). Mice homozygous for the eNOS mutation, heterozygous for Leprdb, and segregating for misty (m) were sent to The Jackson Laboratory. Upon arrival, mice were bred with C57BLKS/J inbred mice (Stock No. 000662) to establish this colony (and remove misty).
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. One marker on Chromosome 5 was still segregating with the targeted mutation. Two markers on Chromosome 11 were found to still be segregating with C57BL/6J as in parental line Stock No. 002684.
Control Suggestions
- BKS.129P2(Cg)-Nos3tm1Unc/J mice (Stock No. 018295) may be an appropriate control.
- 000662 C57BLKS/J
Additional Information
Selected References
- Zhao HJ; Wang S; Cheng H; Zhang MZ; Takahashi T; Fogo AB; Breyer MD; Harris RC. 2006. Endothelial nitric oxide synthase deficiency produces accelerated nephropathy in diabetic mice. J Am Soc Nephrol 17(10):2664-9. PubMed: 16971655MGI: J:135864
Leprdb
Allele Symbol: Leprdb
| Allele Name | diabetes |
|---|---|
| Allele Type | Spontaneous |
| Allele Synonym(s) | Lepdb; Lepr-; Leprdb-1J; db; db/db; leprdb |
| Gene Symbol and Name | Lepr, leptin receptor |
| Gene Synonym(s) | CD295; Fa; LEP-R; LEPRD; LEPROT; Leprb; Modb1; OB-R; OB-RGRP; OBR; Obr; db; diabetes; leptin receptor gene-related protein; obese-like; obese-like; obl; obl |
| Strain of Origin | C57BLKS/J |
| Chromosome | 4 |
| General Note | Phenotypic Similarity to Human Syndrome: Gestational Diabetes J:219658 |
| Molecular Note | A G-to-T transversion in this allele created a donor splice site that causes abnormal splicing and a 106 nt insertion in the transcript, leading to premature termination of the long cellular domain of the Ob-Rb splice form and loss of its signal transducing function. |
Nos3tm1Unc
Allele Symbol: Nos3tm1Unc
| Allele Name | targeted mutation 1, University of North Carolina |
|---|---|
| Allele Type | Targeted (Null/Knockout) |
| Allele Synonym(s) | NOS3-; eNOS-; eNOSKO; ecNOS- |
| Gene Symbol and Name | Nos3, nitric oxide synthase 3, endothelial cell |
| Gene Synonym(s) | 2310065A03Rik; 2310065A03Rik; ECNOS; Nos-3; Nos-3; RIKEN cDNA 2310065A03 gene; eNOS; eNos; ecNOS; nitric oxide synthase 3 (indicible) |
| Strain of Origin | 129P2/OlaHsd |
| Chromosome | 5 |
| Molecular Note | A 1.2 kb neomycin cassette replaced 129 bp of exon 12 of the gene. This disrupted the calmodulin binding site of the protein and introduced a premature stop codon into the transcripts. Immunohistochemisty of heart and kidney sections from homozygous mutant mice confirmed that no detectable encoded protein was present. |
| Mutations Made By | Dr. Oliver Smithies, University of North Carolina at Chapel Hill |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Cardiovascular Research
- Hypertension
- Metabolic Syndrome
- Other
- altered fat metabolism
- altered lipoprotein profile
- Diabetes and Obesity Research
- Hyperglycemia
- Hyperinsulinemia
- Insulin Resistance
- more severe
- Obesity With Diabetes
- severe
- Type 2 Diabetes (NIDDM)
- Endocrine Deficiency Research
- Adipose Defects
- Hypothalamus/Pituitary Defects
- Internal/Organ Research
- Adipose Defects
- Kidney Defects
- Metabolism Research
- Lipid Metabolism
- Research Tools
- Diabetes and Obesity Research
Genotype: Leprdb related
- Diabetes and Obesity Research
- Hyperinsulinemia
- Impaired Wound Healing
- Insulin Resistance
- Obesity With Diabetes
- Endocrine Deficiency Research
- Adipose Defects
- Hypothalamus/Pituitary Defects
- Pancreas Defects
- Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency Associated with Other Defects
- Internal/Organ Research
- Adipose Defects
- Metabolism Research
- Reproductive Biology Research
- Fertility Defects
Genotype: Nos3tm1Unc related
- Cardiovascular Research
- Heart Abnormalities
- bradycardia
- Hypertension
- Heart Abnormalities
- Diabetes and Obesity Research
- Insulin Resistance
- Internal/Organ Research
- Heart Abnormalities
Mammalian Phenotype Terms by Genotype
Genotype: Leprdb/Leprdb Nos3tm1Unc/Nos3tm1Unc
BKS.Cg-Leprdb Nos3tm1Unc
renal/urinary system phenotype
- abnormal kidney afferent arteriole morphology
- arteriolar hyalinosis (MGI Ref ID J:135864)
- abnormal nephron morphology
- (MGI Ref ID J:135864)
- abnormal renal glomerulus morphology
- glomerular injury is significantly increased by 24-26 weeks in comparison to all controls (MGI Ref ID J:135864)
- albuminuria
- albumin/creatinine ratio (ACR) is significantly higher than all controls (MGI Ref ID J:135864)
- decreased renal glomerular filtration rate
- GFR is decreased in comparison to homozygous Nos3tm1Unc and Leprdb controls (MGI Ref ID J:135864)
- expanded mesangial matrix
- marked mesangial expansion is observed at 26 weeks of age (MGI Ref ID J:135864)
- glomerulosclerosis
- focal nodular sclerosis is observed at 26 weeks of age (MGI Ref ID J:135864)
- increased renal glomerulus basement membrane thickness
- glomerular basement membrane is markedly thickened by 16 weeks in comparison to all controls (MGI Ref ID J:135864)
- mesangiolysis
- marked mesangiolysis is observed at 26 weeks of age (MGI Ref ID J:135864)
- renal glomerulus fibrosis
- substantial fibronectin accumulation is observed in glomeruli (MGI Ref ID J:135864)
homeostasis/metabolism phenotype
- albuminuria
- albumin/creatinine ratio (ACR) is significantly higher than all controls (MGI Ref ID J:135864)
- hyperglycemia
- hyperglycemia is first observed between 6-8 weeks of age, but is not higher than homozygous Leprdb control (MGI Ref ID J:135864)
- increased circulating creatinine level
- at 26 weeks, serum creatinine is significantly higher than all controls (MGI Ref ID J:135864)
growth/size/body region phenotype
- increased body weight
- at 26 weeks, body weight is double that of lean and Nos3tm1Unc controls (MGI Ref ID J:135864)
cardiovascular system phenotype
- abnormal kidney afferent arteriole morphology
- arteriolar hyalinosis (MGI Ref ID J:135864)
- increased systemic arterial systolic blood pressure
- hypertension is observed between 24-28 weeks of age, but is not significantly higher than homozygous Nos3tm1Unc controls (MGI Ref ID J:135864)
References
- Zhao HJ; Wang S; Cheng H; Zhang MZ; Takahashi T; Fogo AB; Breyer MD; Harris RC. 2006. Endothelial nitric oxide synthase deficiency produces accelerated nephropathy in diabetic mice. J Am Soc Nephrol 17(10):2664-9. PubMed: 16971655MGI: J:135864
Additional - Leprdb related
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Additional - Nos3tm1Unc related
- Abudukadier A; Fujita Y; Obara A; Ohashi A; Fukushima T; Sato Y; Ogura M; Nakamura Y; Fujimoto S; Hosokawa M; Hasegawa H; Inagaki N. 2013. Tetrahydrobiopterin has a glucose-lowering effect by suppressing hepatic gluconeogenesis in an endothelial nitric oxide synthase-dependent manner in diabetic mice. Diabetes 62(9):3033-43. PubMed: 23649519MGI: J:208962
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- Al Gadban MM; German J; Truman JP; Soodavar F; Riemer EC; Twal WO; Smith KJ; Heller D; Hofbauer AF; Oates JC; Hammad SM. 2012. Lack of nitric oxide synthases increases lipoprotein immune complex deposition in the aorta and elevates plasma sphingolipid levels in lupus. Cell Immunol 276(1-2):42-51. PubMed: 22560558MGI: J:188295
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- Almodovar AJ; Luther RJ; Stonebrook CL; Wood PA. 2013. Genomic structure and genetic drift in C57BL/6 congenic metabolic mutant mice. Mol Genet Metab 110(3):396-400. PubMed: 23867526MGI: J:205314
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- Bergula AP; Haidekker MA; Huang W; Stevens HY; Frangos JA. 2004. Venous ligation-mediated bone adaptation is NOS 3 dependent. Bone 34(3):562-9. PubMed: 15003804MGI: J:109405
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