About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Nos3tm1Unc
targeted mutation 1, University of North Carolina
MGI:1857229
Summary 12 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Nos3tm1Unc/Nos3tm1Unc B6.129P2-Nos3tm1Unc MGI:4834530
hm2
Nos3tm1Unc/Nos3tm1Unc B6.129P2-Nos3tm1Unc/J MGI:3618597
hm3
Nos3tm1Unc/Nos3tm1Unc BKS.129P2-Nos3tm1Unc MGI:4361716
hm4
Nos3tm1Unc/Nos3tm1Unc involves: 129P2/OlaHsd MGI:3618625
hm5
Nos3tm1Unc/Nos3tm1Unc involves: 129P2/OlaHsd * C57BL/6 MGI:2174981
hm6
Nos3tm1Unc/Nos3tm1Unc involves: 129P2/OlaHsd * C57BL/6J MGI:3630164
ht7
Nos3tm1Unc/Nos3+ B6.129P2-Nos3tm1Unc/J MGI:5427346
ht8
Nos3tm1Unc/Nos3+ involves: 129P2/OlaHsd * C57BL/6J MGI:3630165
cx9
Apoetm1Unc/Apoetm1Unc
Nos3tm1Unc/Nos3tm1Unc
B6.129P2-Nos3tm1Unc Apoetm1Unc MGI:3794764
cx10
Nos2tm1Lau/Nos2tm1Lau
Nos3tm1Unc/Nos3tm1Unc
B6.129P2-Nos3tm1Unc Nos2tm1Lau MGI:4367219
cx11
Leprdb/Leprdb
Nos3tm1Unc/Nos3tm1Unc
BKS.Cg-Leprdb Nos3tm1Unc MGI:4361710
cx12
Nos1tm1Plh/Nos1tm1Plh
Nos3tm1Unc/Nos3tm1Unc
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J MGI:4367218


Genotype
MGI:4834530
hm1
Allelic
Composition
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
B6.129P2-Nos3tm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• kainic acid injection of hippocampi does not cause blood-brain barrier breakdown (J:150557)
• kainic acid injection of hippocampi does not cause blood-brain barrier breakdown (J:150557)

nervous system
• kainic acid injection of hippocampi does not cause blood-brain barrier breakdown (J:150557)
• kainic acid injection of hippocampi does not cause blood-brain barrier breakdown (J:150557)




Genotype
MGI:3618597
hm2
Allelic
Composition
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
B6.129P2-Nos3tm1Unc/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 40% die within the first hour of birth (J:98913)
• about 40% die within the first hour of birth (J:98913)
• 85% of mice die by P10 compared with 13% of wild-type mice (J:103270)
• 85% of mice die by P10 compared with 13% of wild-type mice (J:103270)

growth/size/body
• fetuses from E18 to term demonstrate slight growth retardation (J:98913)
• fetuses from E18 to term demonstrate slight growth retardation (J:98913)
• Intrauterine Growth Retardation demonstrated by ultrasonographic imaging showing differences in embryo and gestational vesicle measurements in both longitudinal and transversal curves from Days 5.5 to 14.5. (J:140819)
• Intrauterine Growth Retardation demonstrated by ultrasonographic imaging showing differences in embryo and gestational vesicle measurements in both longitudinal and transversal curves from Days 5.5 to 14.5. (J:140819)

cardiovascular system
• after remnant kidney surgery, homozygotes exhibit a significantly greater endothelial cell loss than similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly greater endothelial cell loss than similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly greater decrease (50%) in endothelial cell density in the glomeruli and renal cortex relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly greater decrease (50%) in endothelial cell density in the glomeruli and renal cortex relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop microaneurysms unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop microaneurysms unlike similarly-treated wild-type controls (J:148626)
• abnormalities in pulmonary vascular development (J:98913)
• disorganization of the extracellular matrix structure in the lung vasculature (J:98913)
• capillaries of preterm mice remain deep within thickened septae, instead of aligning with the saccular epithelium, resulting in significantly fewer capillaries abutting saccular airspaces (J:98913)
• abnormalities in pulmonary vascular development (J:98913)
• disorganization of the extracellular matrix structure in the lung vasculature (J:98913)
• capillaries of preterm mice remain deep within thickened septae, instead of aligning with the saccular epithelium, resulting in significantly fewer capillaries abutting saccular airspaces (J:98913)
• severe with focal alveolar edema (J:103270)
• severe with focal alveolar edema (J:103270)
• impaired pulmonary angiogenesis (J:98913)
• occasionally exhibit misalignment of pulmonary veins, which are seen in anomalous locations adjacent to the lung pleura, running alongside arterial vessels and sharing a common adventitial sheath (J:98913)
• impaired pulmonary angiogenesis (J:98913)
• occasionally exhibit misalignment of pulmonary veins, which are seen in anomalous locations adjacent to the lung pleura, running alongside arterial vessels and sharing a common adventitial sheath (J:98913)
• E19.5 lungs show dramatic decrease of arteriolar branches and regions of marked capillary hypoperfusion (J:98913)
• E19.5 lungs show dramatic decrease of arteriolar branches and regions of marked capillary hypoperfusion (J:98913)
• diastolic dimension is increased compared to in wild-type mice (J:103270)
• diastolic dimension is increased compared to in wild-type mice (J:103270)
• membranous and muscular ventricular defects in 6 of 10 mice compared with 1 of 10 atrial septal defects in wild-type mice (J:103270)
• membranous and muscular ventricular defects in 6 of 10 mice compared with 1 of 10 atrial septal defects in wild-type mice (J:103270)
• in response to transverse aortic constriction (TAC)-induced pressure overload, wild-type hearts exhibit a progressive cardiac hypertrophy with significant dilatory remodeling whereas mutant hearts show more modest and concentric cardiac hypertrophy at 3 weeks, with minimal further progression (J:98094)
• at 9 weeks after TAC, mutant hearts develop significantly less intestitial fibrosis, myocyte hypertrophy, and fetal gene re-expression (B-natriuretic peptide and alpha-skeletal actin) relative wild-type hearts (J:98094)
• however, homozygotes show no significant differences in baseline heart weight or myocyte size relative to wild-type mice (J:98094)
• in response to transverse aortic constriction (TAC)-induced pressure overload, wild-type hearts exhibit a progressive cardiac hypertrophy with significant dilatory remodeling whereas mutant hearts show more modest and concentric cardiac hypertrophy at 3 weeks, with minimal further progression (J:98094)
• at 9 weeks after TAC, mutant hearts develop significantly less intestitial fibrosis, myocyte hypertrophy, and fetal gene re-expression (B-natriuretic peptide and alpha-skeletal actin) relative wild-type hearts (J:98094)
• however, homozygotes show no significant differences in baseline heart weight or myocyte size relative to wild-type mice (J:98094)
• high incidence (5 of 12) bicuspid aortic valves, however do not exhibit aortic coarctation (J:103340)
• high incidence (5 of 12) bicuspid aortic valves, however do not exhibit aortic coarctation (J:103340)
• ventricular hypertrophy (J:103270)
• ventricular hypertrophy (J:103270)
• E16 lungs show scattered areas of parenchymal and interlobar hemorrhages (J:98913)
• E16 lungs show scattered areas of parenchymal and interlobar hemorrhages (J:98913)
• at 9 weeks of TAC, wild-type hearts exhibit a rightward shift of LV pressure-volume (PV) loops and end-systolic and end-diastolic PV relations reflecting remodeling; in contrast, mutant hearts display a leftward shift with smaller end-diastolic and end-systolic chamber volumes, as well as preserved wall thickness and fractional shortening, indicating preserved or enhanced systolic and diastolic function (J:98094)
• at 9 weeks of TAC, wild-type hearts exhibit a rightward shift of LV pressure-volume (PV) loops and end-systolic and end-diastolic PV relations reflecting remodeling; in contrast, mutant hearts display a leftward shift with smaller end-diastolic and end-systolic chamber volumes, as well as preserved wall thickness and fractional shortening, indicating preserved or enhanced systolic and diastolic function (J:98094)
• in fetal atrioventricular endothelial cushions, septum primum and right and left ventricular myocardium (J:103270)
• at E12.5, E15.5 and P1 in the myocardium (J:103270)
• in fetal atrioventricular endothelial cushions, septum primum and right and left ventricular myocardium (J:103270)
• at E12.5, E15.5 and P1 in the myocardium (J:103270)
• in response to TAC-induced pressure overload, homozygotes exhibit a similar or greater rise in LV systolic pressure and ventricular afterload (arterial elastance [Ea]) at 9 weeks relative to wild-type mice (J:98094)
• in response to TAC-induced pressure overload, homozygotes exhibit a similar or greater rise in LV systolic pressure and ventricular afterload (arterial elastance [Ea]) at 9 weeks relative to wild-type mice (J:98094)
• at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes fail to exhibit a further increase in systolic blood pressure relative to sham-operated homozygotes, unlike wild-type controls (J:148626)
• at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes fail to exhibit a further increase in systolic blood pressure relative to sham-operated homozygotes, unlike wild-type controls (J:148626)

respiratory system
• E16 lungs show scattered areas of parenchymal and interlobar hemorrhages (J:98913)
• E16 lungs show scattered areas of parenchymal and interlobar hemorrhages (J:98913)
• fetal lungs demonstrate abnormally compact lung structure and lungs of pups show evidence of septal thickening and reduced airspaces (J:98913)
• E20 lungs display absence of discernible basement membrane in the distal airways (J:98913)
• exhibit a decrease in apoptosis in the lungs (J:98913)
• E16 lungs display scattered subpleural hematomas (J:98913)
• fetal lungs demonstrate abnormally compact lung structure and lungs of pups show evidence of septal thickening and reduced airspaces (J:98913)
• E20 lungs display absence of discernible basement membrane in the distal airways (J:98913)
• exhibit a decrease in apoptosis in the lungs (J:98913)
• E16 lungs display scattered subpleural hematomas (J:98913)
• abnormalities in pulmonary vascular development (J:98913)
• disorganization of the extracellular matrix structure in the lung vasculature (J:98913)
• capillaries of preterm mice remain deep within thickened septae, instead of aligning with the saccular epithelium, resulting in significantly fewer capillaries abutting saccular airspaces (J:98913)
• abnormalities in pulmonary vascular development (J:98913)
• disorganization of the extracellular matrix structure in the lung vasculature (J:98913)
• capillaries of preterm mice remain deep within thickened septae, instead of aligning with the saccular epithelium, resulting in significantly fewer capillaries abutting saccular airspaces (J:98913)
• severe with focal alveolar edema (J:103270)
• severe with focal alveolar edema (J:103270)
• observe an increase in markedly swollen glycogen laden pneumocytes protruding into airspaces compared to wild-type (J:98913)
• observe an increase in markedly swollen glycogen laden pneumocytes protruding into airspaces compared to wild-type (J:98913)
• no evidence of lamellar bodies in type II pneumocytes (J:98913)
• no evidence of lamellar bodies in type II pneumocytes (J:98913)
• pups exhibit marked septal thickening (J:98913)
• pups exhibit marked septal thickening (J:98913)
• some newborns exhibit severe respiratory distress (J:98913)
• some newborns exhibit severe respiratory distress (J:98913)
• lack of surfactant in bronchial alveolar lavage fluid (J:103340)
• lack of surfactant in bronchial alveolar lavage fluid (J:103340)

homeostasis/metabolism
• after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly higher increase in BUN levels relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly higher increase in BUN levels relative to similarly-treated wild-type controls (J:148626)
• serum osteocalcin (BGLAP) levels are significantly higher in sham treated compared to wild-type sham mice at baseline, 14 weeks and remained higher (J:129477)
• serum TRAP5b (ACP5) concentrations are significantly higher in sham treated compared wild-type sham treated mice at all time points (J:129477)
• serum osteocalcin (BGLAP) levels are significantly higher in sham treated compared to wild-type sham mice at baseline, 14 weeks and remained higher (J:129477)
• serum TRAP5b (ACP5) concentrations are significantly higher in sham treated compared wild-type sham treated mice at all time points (J:129477)
• after remnant kidney surgery, homozygotes exhibit a significantly higher increase in serum creatinine levels relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly higher increase in serum creatinine levels relative to similarly-treated wild-type controls (J:148626)
• some newborns show varying levels of cyanosis (J:98913)
• some newborns show varying levels of cyanosis (J:98913)
• after remnant kidney surgery, homozygotes exhibit a significantly higher increase in urinary albumin excretion relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly higher increase in urinary albumin excretion relative to similarly-treated wild-type controls (J:148626)

muscle
• at 9 weeks of TAC, wild-type hearts exhibit a rightward shift of LV pressure-volume (PV) loops and end-systolic and end-diastolic PV relations reflecting remodeling; in contrast, mutant hearts display a leftward shift with smaller end-diastolic and end-systolic chamber volumes, as well as preserved wall thickness and fractional shortening, indicating preserved or enhanced systolic and diastolic function (J:98094)
• at 9 weeks of TAC, wild-type hearts exhibit a rightward shift of LV pressure-volume (PV) loops and end-systolic and end-diastolic PV relations reflecting remodeling; in contrast, mutant hearts display a leftward shift with smaller end-diastolic and end-systolic chamber volumes, as well as preserved wall thickness and fractional shortening, indicating preserved or enhanced systolic and diastolic function (J:98094)

cellular
• in fetal atrioventricular endothelial cushions, septum primum and right and left ventricular myocardium (J:103270)
• at E12.5, E15.5 and P1 in the myocardium (J:103270)
• in fetal atrioventricular endothelial cushions, septum primum and right and left ventricular myocardium (J:103270)
• at E12.5, E15.5 and P1 in the myocardium (J:103270)
• at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes exhibit a 4.6-fold increase in peritubular endothelial cell apoptosis relative to similarly-treated wild-type controls (J:148626)
• at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes exhibit a 4.6-fold increase in peritubular endothelial cell apoptosis relative to similarly-treated wild-type controls (J:148626)
• in two week old mice based upon TUNEL staining and the presence of Apoptotic nuclei with a dense punctate appearance (J:117046)
• in two week old mice based upon TUNEL staining and the presence of Apoptotic nuclei with a dense punctate appearance (J:117046)
• after remnant kidney surgery, homozygotes exhibit a 36% reduction of proliferating endothelial cells in cortical peritubular capillaries relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a 36% reduction of proliferating endothelial cells in cortical peritubular capillaries relative to similarly-treated wild-type controls (J:148626)
• in response to TAC-induced pressure overload, homozygotes (but not wild-type mice) exhibit blunted myocardial ROS generation and blunted nitrotyrosine, and gelatinase zymogen activity with no significant decline in the GSH/GSSH or NADPH/NADP ratio (J:98094)
• in response to TAC-induced pressure overload, homozygotes (but not wild-type mice) exhibit blunted myocardial ROS generation and blunted nitrotyrosine, and gelatinase zymogen activity with no significant decline in the GSH/GSSH or NADPH/NADP ratio (J:98094)

endocrine/exocrine glands
• on day 0.5 of estrous cycle, mutant ovaries display a scarce number of ovulation sites and a higher number of anovulatory and luteinized unruptured follicles relative to wild-type controls (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries display a scarce number of ovulation sites and a higher number of anovulatory and luteinized unruptured follicles relative to wild-type controls (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries exhibit significantly less corpora lutea than wild-type ovaries (9.7 +/- 1.2 versus 14.2 +/- 1.2, respectively) (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries exhibit significantly less corpora lutea than wild-type ovaries (9.7 +/- 1.2 versus 14.2 +/- 1.2, respectively) (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries are significantly smaller than wild-type (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries are significantly smaller than wild-type (J:145649)

reproductive system
• on day 0.5 of estrous cycle, mutant ovaries display a scarce number of ovulation sites and a higher number of anovulatory and luteinized unruptured follicles relative to wild-type controls (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries display a scarce number of ovulation sites and a higher number of anovulatory and luteinized unruptured follicles relative to wild-type controls (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries exhibit significantly less corpora lutea than wild-type ovaries (9.7 +/- 1.2 versus 14.2 +/- 1.2, respectively) (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries exhibit significantly less corpora lutea than wild-type ovaries (9.7 +/- 1.2 versus 14.2 +/- 1.2, respectively) (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries are significantly smaller than wild-type (J:145649)
• on day 0.5 of estrous cycle, mutant ovaries are significantly smaller than wild-type (J:145649)
• female homozygotes display a higher rate of anovulation than wild-type controls (48.3 +/- 7.3% versus 29.7 +/- 6.3, respectively) (J:145649)
• female homozygotes display a higher rate of anovulation than wild-type controls (48.3 +/- 7.3% versus 29.7 +/- 6.3, respectively) (J:145649)
• female homozygotes display a lower ovulation rate than wild-type controls (9.7 +/- 1.2% versus 14.2 +/- 1.2%, respectively) (J:145649)
• female homozygotes display a lower ovulation rate than wild-type controls (9.7 +/- 1.2% versus 14.2 +/- 1.2%, respectively) (J:145649)
• mutant dams show a higher incidence of embryo losses than wild-type dams (62.5% versus 16.7%, respectively) (J:145649)
• the mean rate of embryo losses detected in mutant dams is 49.90.1% versus less than 20% in wild-type dams (J:145649)
• in mutant dams, the highest %s of embryo losses occur between days 8.5 and 10.5 (55.6%) and at day 13.5 postcoitum (44.4% of total losses), whereas in control dams embryo losses occur at days 10.5 and 11.5 postcoitum (J:145649)
• mutant dams show a higher incidence of embryo losses than wild-type dams (62.5% versus 16.7%, respectively) (J:145649)
• the mean rate of embryo losses detected in mutant dams is 49.90.1% versus less than 20% in wild-type dams (J:145649)
• in mutant dams, the highest %s of embryo losses occur between days 8.5 and 10.5 (55.6%) and at day 13.5 postcoitum (44.4% of total losses), whereas in control dams embryo losses occur at days 10.5 and 11.5 postcoitum (J:145649)
• on days 6.5 and 8.5 of pregnancy, the average number of embryos reaching implantation is lower in mutant mice relative to wild-type mice (4.0 +/- 0.4 versus 7.5 +/- 0.4, respectively) (J:145649)
• on days 6.5 and 8.5 of pregnancy, the average number of embryos reaching implantation is lower in mutant mice relative to wild-type mice (4.0 +/- 0.4 versus 7.5 +/- 0.4, respectively) (J:145649)
• on day 0.5 of estrous cycle, female homozygotes show a significant reduction in the total number of recovered embryos (oocytes/zygotes) relative to wild-type controls (4.0 +/- 1.1 versus 10.4 +/- 1.6, respectively) (J:145649)
• thereafter, a mean of 2.0 +/- 1.0 of these recovered embryos are found to be fertilized, representing a non-fertilization rate of 50.7% versus only 3.3% in control littermates (J:145649)
• on day 0.5 of estrous cycle, female homozygotes show a significant reduction in the total number of recovered embryos (oocytes/zygotes) relative to wild-type controls (4.0 +/- 1.1 versus 10.4 +/- 1.6, respectively) (J:145649)
• thereafter, a mean of 2.0 +/- 1.0 of these recovered embryos are found to be fertilized, representing a non-fertilization rate of 50.7% versus only 3.3% in control littermates (J:145649)

immune system
• serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points (J:129477)
• serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points (J:129477)
• fever in response to turpentine injection is enhanced compared to wild-type controls (J:103018)
• unlike in mice null for either Nos1 or Nos2, fever in response to LPS injection is not significantly different from wild-type controls (J:103018)
• fever in response to turpentine injection is enhanced compared to wild-type controls (J:103018)
• unlike in mice null for either Nos1 or Nos2, fever in response to LPS injection is not significantly different from wild-type controls (J:103018)
• after remnant kidney surgery, homozygotes exhibit increased macrophage infiltration in the glomeruli (15.4-fold) and in the tubulointerstitium (2.7-fold) relative to similarly-treated wild-type controls (J:148626)
• however, a similar increase in glomerular T-cell infiltration (62%) is seen in both RK groups (J:148626)
• after remnant kidney surgery, homozygotes exhibit increased macrophage infiltration in the glomeruli (15.4-fold) and in the tubulointerstitium (2.7-fold) relative to similarly-treated wild-type controls (J:148626)
• however, a similar increase in glomerular T-cell infiltration (62%) is seen in both RK groups (J:148626)

renal/urinary system
• at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes exhibit a 4.6-fold increase in peritubular endothelial cell apoptosis relative to similarly-treated wild-type controls (J:148626)
• at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes exhibit a 4.6-fold increase in peritubular endothelial cell apoptosis relative to similarly-treated wild-type controls (J:148626)
• in two week old mice based upon TUNEL staining and the presence of Apoptotic nuclei with a dense punctate appearance (J:117046)
• in two week old mice based upon TUNEL staining and the presence of Apoptotic nuclei with a dense punctate appearance (J:117046)
• after remnant kidney surgery, homozygotes exhibit a 36% reduction of proliferating endothelial cells in cortical peritubular capillaries relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a 36% reduction of proliferating endothelial cells in cortical peritubular capillaries relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly higher increase in urinary albumin excretion relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly higher increase in urinary albumin excretion relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit increased macrophage infiltration in the glomeruli (15.4-fold) and in the tubulointerstitium (2.7-fold) relative to similarly-treated wild-type controls (J:148626)
• however, a similar increase in glomerular T-cell infiltration (62%) is seen in both RK groups (J:148626)
• after remnant kidney surgery, homozygotes exhibit increased macrophage infiltration in the glomeruli (15.4-fold) and in the tubulointerstitium (2.7-fold) relative to similarly-treated wild-type controls (J:148626)
• however, a similar increase in glomerular T-cell infiltration (62%) is seen in both RK groups (J:148626)
• in 80% of adult freshly isolated kidneys indentations are observed, indicating zones of parenchymal scarring (J:117046)
• 4% of glomeruli outside scarred area exhibit loss of cellularity and vasculature, a hyalinization like appearance (J:117046)
• in 80% of adult freshly isolated kidneys indentations are observed, indicating zones of parenchymal scarring (J:117046)
• 4% of glomeruli outside scarred area exhibit loss of cellularity and vasculature, a hyalinization like appearance (J:117046)
• after remnant kidney surgery, homozygotes develop microaneurysms unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop microaneurysms unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a 44% increase in tubulointerstitial injury relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a 44% increase in tubulointerstitial injury relative to similarly-treated wild-type controls (J:148626)
• glomeruli within scarred areas are considerably smaller than wild-type (J:117046)
• glomeruli within scarred areas are considerably smaller than wild-type (J:117046)
• after remnant kidney surgery, homozygotes exhibit a significantly greater endothelial cell loss than similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a significantly greater endothelial cell loss than similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit increased mesangial proliferation relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit increased mesangial proliferation relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit increased matrix deposition in some glomeruli unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit increased matrix deposition in some glomeruli unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop mesangiolysis unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop mesangiolysis unlike similarly-treated wild-type controls (J:148626)
• within scarred areas (J:117046)
• within scarred areas (J:117046)
• after remnant kidney surgery, homozygotes develop significant glomerulosclerosis, unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop significant glomerulosclerosis, unlike similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a 46% increase in glomerular collagen IV deposition relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a 46% increase in glomerular collagen IV deposition relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop significantly greater glomerular hypertrophy than similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes develop significantly greater glomerular hypertrophy than similarly-treated wild-type controls (J:148626)
• frequently a large lipid droplet is observed with Bowman's capsule and the adjacent matrix (J:117046)
• frequently a large lipid droplet is observed with Bowman's capsule and the adjacent matrix (J:117046)
• after remnant kidney surgery, homozygotes exhibit more severe sloughing , vacuolization and nuclear exfoliation of tubular epithelial cells relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit more severe sloughing , vacuolization and nuclear exfoliation of tubular epithelial cells relative to similarly-treated wild-type controls (J:148626)
• thin strands of connective tissue distributed loosely within the interglomerular interstitium (J:117046)
• thin strands of connective tissue distributed loosely within the interglomerular interstitium (J:117046)
• after remnant kidney surgery, homozygotes exhibit a 38% increase in collagen III deposition in the tubulointerstitium relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit a 38% increase in collagen III deposition in the tubulointerstitium relative to similarly-treated wild-type controls (J:148626)
• within scarred areas (J:117046)
• within scarred areas (J:117046)
• the glomeruli often display no clear connection to typical large-diameter proximal tubules (J:117046)
• the glomeruli often display no clear connection to typical large-diameter proximal tubules (J:117046)
• after remnant kidney surgery, homozygotes exhibit more severe tubular dilatation than similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit more severe tubular dilatation than similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit more severe tubular cast formation than similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit more severe tubular cast formation than similarly-treated wild-type controls (J:148626)
• degeneration of the glomerular core components is common within the scarred zones (J:117046)
• degeneration of the glomerular core components is common within the scarred zones (J:117046)
• in 2 week old mice, as pyknotic nuclei and vacuolated cytoplasm are observed (J:117046)
• in 2 week old mice, as pyknotic nuclei and vacuolated cytoplasm are observed (J:117046)
• after remnant kidney surgery, homozygotes exhibit significantly worse renal function relative to similarly-treated wild-type controls (J:148626)
• after remnant kidney surgery, homozygotes exhibit significantly worse renal function relative to similarly-treated wild-type controls (J:148626)

skeleton
• serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points (J:129477)
• serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points (J:129477)
• exagerated BMD decrease in ovariectomized mice (J:129477)
• exagerated BMD decrease in ovariectomized mice (J:129477)
• between 10-20 weeks post sham-operation compared to sham-operated wild-type (J:129477)
• between 10-20 weeks post sham-operation compared to sham-operated wild-type (J:129477)
• significantly greater cortical thickness in sham operated mice compared to sham operated wild-type mice (J:129477)
• significantly greater cortical thickness in sham operated mice compared to sham operated wild-type mice (J:129477)
• serum osteocalcin (BGLAP) levels are significantly higher in sham compared wit wild-type sham mice at baseline and at 14 wk and remained higher (J:129477)
• serum osteocalcin (BGLAP) levels are significantly higher in sham compared wit wild-type sham mice at baseline and at 14 wk and remained higher (J:129477)

hematopoietic system
• serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points (J:129477)
• serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points (J:129477)




Genotype
MGI:4361716
hm3
Allelic
Composition
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
BKS.129P2-Nos3tm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• moderate albuminuria is observed at 26 weeks of age (J:135864)
• moderate albuminuria is observed at 26 weeks of age (J:135864)

homeostasis/metabolism
• moderate albuminuria is observed at 26 weeks of age (J:135864)
• moderate albuminuria is observed at 26 weeks of age (J:135864)

cardiovascular system
• observed by 24 to 28 weeks of age (J:135864)
• observed by 24 to 28 weeks of age (J:135864)




Genotype
MGI:3618625
hm4
Allelic
Composition
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% of males die by 21 months of age, however female survival is similar to wild-type (J:102136)
• 50% of males die by 21 months of age, however female survival is similar to wild-type (J:102136)

growth/size/body
• both males and females weight less than wild-type at 21 months of age (J:102136)
• both males and females weight less than wild-type at 21 months of age (J:102136)

cardiovascular system
• at 21 months of age, males exhibit wall thinning of the heart while females display an increase in wall thickness of the heart (J:102136)
• at 21 months of age, males exhibit wall thinning of the heart while females display an increase in wall thickness of the heart (J:102136)
• females, but not males, exhibit a significant increase in diastolic septal wall thickness and to a lesser degree in the posterior wall (J:102136)
• males exhibit a decrease in interventricular septum thickening at 21 months of age (J:102136)
• females, but not males, exhibit a significant increase in diastolic septal wall thickness and to a lesser degree in the posterior wall (J:102136)
• males exhibit a decrease in interventricular septum thickening at 21 months of age (J:102136)
• large increase in heart weight and heart weight to body weight ratio in males at 21 months of age and a smaller increase in females (J:102136)
• large increase in heart weight and heart weight to body weight ratio in males at 21 months of age and a smaller increase in females (J:102136)
• at 21 months of age, males have a large increase and females have a slight increase in heart size (J:102136)
• at 21 months of age, males have a large increase and females have a slight increase in heart size (J:102136)
• left-ventricular end-systolic chamber dilation (LVESD) is increased about 45% in homozygous males compared to 25% in wild-type males at 21 months of age; no differences seen in females (J:102136)
• left ventricular mass (LVMASS) is increased in both males and females at 21 months of age (J:102136)
• ratio between LVMASS and LV volume is increased in 21 month old males (J:102136)
• left-ventricular end-systolic chamber dilation (LVESD) is increased about 45% in homozygous males compared to 25% in wild-type males at 21 months of age; no differences seen in females (J:102136)
• left ventricular mass (LVMASS) is increased in both males and females at 21 months of age (J:102136)
• ratio between LVMASS and LV volume is increased in 21 month old males (J:102136)
• males at 21 months of age, but not at 5.5 months, exhibit a decrease in left ventricular posterior wall (J:102136)
• males at 21 months of age, but not at 5.5 months, exhibit a decrease in left ventricular posterior wall (J:102136)
• insulin stimulation of muscle blood flow is about 40% smaller than in wild-type (J:103153)
• insulin stimulation of muscle blood flow is about 40% smaller than in wild-type (J:103153)
• males, but not females, exhibit a marked decrease in ejection fraction and shortening fraction at 21 months of age (J:102136)
• males, but not females, exhibit a marked decrease in ejection fraction and shortening fraction at 21 months of age (J:102136)
• heart rate is increased in males at 5.5 months of age but not at 21 months of age (J:102136)
• heart rate is normal in females at 5.5 months of age but remains elevated at 21 months of age and does not fall with age as in wild-type (J:102136)
• heart rate is increased in males at 5.5 months of age but not at 21 months of age (J:102136)
• heart rate is normal in females at 5.5 months of age but remains elevated at 21 months of age and does not fall with age as in wild-type (J:102136)
• mean blood pressure is significantly elevated in both males and females at 5.5 months of age (J:102136)
• at 21 months of age, females, but not males, continue to exhibit increased mean blood pressure (J:102136)
• mean blood pressure is significantly elevated in both males and females at 5.5 months of age (J:102136)
• at 21 months of age, females, but not males, continue to exhibit increased mean blood pressure (J:102136)
• females are hypertensive at 7 months of age and maintain the elevated pressure at 21 months of age, however do not exhibit any contractile dysfunction (J:102136)
• females are hypertensive at 7 months of age and maintain the elevated pressure at 21 months of age, however do not exhibit any contractile dysfunction (J:102136)
• arterial hypertension (J:103153)
• arterial hypertension (J:103153)
• elevated at 5.5 months of age in both males and females (J:102136)
• at 21 months of age, females, but not males, continue to exhibit an increased diastolic blood pressure (J:102136)
• elevated at 5.5 months of age in both males and females (J:102136)
• at 21 months of age, females, but not males, continue to exhibit an increased diastolic blood pressure (J:102136)
• elevated at 5.5 months of age in both males and females (J:102136)
• at 21 months of age, females, but not males, continue to exhibit an increased systolic blood pressure (J:102136)
• elevated at 5.5 months of age in both males and females (J:102136)
• at 21 months of age, females, but not males, continue to exhibit an increased systolic blood pressure (J:102136)

homeostasis/metabolism
• plasma nitrite and nitrate concentrations are about 60% lower than in wild-type, indicating a defect of vascular NO production (J:103153)
• plasma nitrite and nitrate concentrations are about 60% lower than in wild-type, indicating a defect of vascular NO production (J:103153)
• insulin-resistant homozygotes have 50% higher plasma levels of cholesterol (J:103153)
• insulin-resistant homozygotes have 50% higher plasma levels of cholesterol (J:103153)
• insulin-resistant homozygotes have a 2-fold elevation of free fatty acid (J:103153)
• insulin-resistant homozygotes have a 2-fold elevation of free fatty acid (J:103153)
• insulin-resistant homozygotes have a 2-fold elevation of triglycerides (J:103153)
• insulin-resistant homozygotes have a 2-fold elevation of triglycerides (J:103153)
• glucose infusion rate, glucose turnover rate, and glucose clearance rate are 30-40% lower during a hyperinsulinemic euglycemic clamp study (J:103153)
• basal and insulin-stimulated glucose transport in isolated skeletal muscle is about 40% lower than in wild-type (J:103153)
• glucose infusion rate, glucose turnover rate, and glucose clearance rate are 30-40% lower during a hyperinsulinemic euglycemic clamp study (J:103153)
• basal and insulin-stimulated glucose transport in isolated skeletal muscle is about 40% lower than in wild-type (J:103153)
• fasting plasma insulin concentration is elevated almost 2-fold (J:103153)
• fasting plasma insulin concentration is elevated almost 2-fold (J:103153)
• fasting hyperinsulinemia and glucose infusion rates during euglycemic clamp studies are 40% lower than in wild-type (J:103153)
• fasting hyperinsulinemia and glucose infusion rates during euglycemic clamp studies are 40% lower than in wild-type (J:103153)

muscle
• insulin stimulation of muscle blood flow is about 40% smaller than in wild-type (J:103153)
• insulin stimulation of muscle blood flow is about 40% smaller than in wild-type (J:103153)
• males, but not females, exhibit a marked decrease in ejection fraction and shortening fraction at 21 months of age (J:102136)
• males, but not females, exhibit a marked decrease in ejection fraction and shortening fraction at 21 months of age (J:102136)

Mouse Models of Human Disease
OMIM ID Ref(s)
Hypertension, Essential 145500 J:103153




Genotype
MGI:2174981
hm5
Allelic
Composition
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• after injection of platelet-activating factor (PAF), less than 10% mortality occurs within 30 minutes (J:113106)
• pretreatment with wortmannin before PAF treatment confers 100% protection to mutants and wild-type (J:113106)
• in BSA-induced anaphylaxis, all mutants survive compared to fatality in 82% of controls; in OVA model, 92% of control mice die but all mutants survive challenge (J:113106)
• after injection of platelet-activating factor (PAF), less than 10% mortality occurs within 30 minutes (J:113106)
• pretreatment with wortmannin before PAF treatment confers 100% protection to mutants and wild-type (J:113106)
• in BSA-induced anaphylaxis, all mutants survive compared to fatality in 82% of controls; in OVA model, 92% of control mice die but all mutants survive challenge (J:113106)

growth/size/body
• body weights at 14 weeks of age are approximately 7.5% lower than in wild-type (J:36559)
• body weights at 14 weeks of age are approximately 7.5% lower than in wild-type (J:36559)
• body weight is signifcantly lower than controls at 14 days of age (J:101254)
• body weight is signifcantly lower than controls at 14 days of age (J:101254)

homeostasis/metabolism
• plasma renin concentrations are nearly twice as high as in wild-type (J:36559)
• plasma renin concentrations are nearly twice as high as in wild-type (J:36559)
• challenge with BSA 2 weeks after sensitization with BSA induces severe hypothermia and mice succumb to systemic shock reaction; mutants show no mortality and only a delayed, mild, transient hypothermia (J:113106)
• similar results are seen with OVA-induced anaphylaxis (J:113106)
• challenge with BSA 2 weeks after sensitization with BSA induces severe hypothermia and mice succumb to systemic shock reaction; mutants show no mortality and only a delayed, mild, transient hypothermia (J:113106)
• similar results are seen with OVA-induced anaphylaxis (J:113106)

cardiovascular system
• larger than in controls but only at 14 day (J:101254)
• medial wall area is greater than in controls in the fetus (J:101254)
• muscularity decreases after birth (J:101254)
• muscularity is reduced in the male but still greater than controls (J:101254)
• muscularity in females is like controls by 14 days of age (J:101254)
• larger than in controls but only at 14 day (J:101254)
• medial wall area is greater than in controls in the fetus (J:101254)
• muscularity decreases after birth (J:101254)
• muscularity is reduced in the male but still greater than controls (J:101254)
• muscularity in females is like controls by 14 days of age (J:101254)
• right ventricle/body weight ratio increased in males (J:101254)
• right ventricle/left ventricle+septum ratio increased in males (J:101254)
• right ventricle/body weight ratio increased in males (J:101254)
• right ventricle/left ventricle+septum ratio increased in males (J:101254)
• in BSA/BSA model of anaphylaxis, vascular permeability increased significantly in wild-type but very little in mutants; vascular leakage (extravasation) of Evans Blue dye (EB) is 2-fold lower than in wild-type mice (J:113106)
• in OVA/OVA model, no vascular permeability increase occurs in mutants and extravasation is significantly lower than in wild-type (J:113106)
• in BSA/BSA model of anaphylaxis, vascular permeability increased significantly in wild-type but very little in mutants; vascular leakage (extravasation) of Evans Blue dye (EB) is 2-fold lower than in wild-type mice (J:113106)
• in OVA/OVA model, no vascular permeability increase occurs in mutants and extravasation is significantly lower than in wild-type (J:113106)
• mean right ventricular pressure is elevated in males but not in females (J:101254)
• mean right ventricular pressure is elevated in males but not in females (J:101254)
• 670 beats per min vs. 709 beats per min in wild-type (J:36559)
• 670 beats per min vs. 709 beats per min in wild-type (J:36559)
• elevated in males but not in females (J:101254)
• elevated in males but not in females (J:101254)

immune system
N
• exhibit a similar susceptibility to lipopolysaccharide-induced death as wild-type (J:36559)
• exhibit a similar susceptibility to lipopolysaccharide-induced death as wild-type (J:36559)




Genotype
MGI:3630164
hm6
Allelic
Composition
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• aortic rings isolated from homozygous mutant mice exhibit a significantly enhanced vasoconstriction in response to phenylephrine and a modestly enhanced vasoconstriction in response to serotonin (J:54772)
• aortic rings isolated from homozygous mutant mice exhibit a significantly enhanced vasoconstriction in response to phenylephrine and a modestly enhanced vasoconstriction in response to serotonin (J:54772)
• aortic rings isolated from homozygous mutant mice show complete loss of endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187 (J:54772)
• in contrast, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are enhanced resulting in a shift of EC50 by ~7-fold relative to wild-type values (J:54772)
• aortic rings isolated from homozygous mutant mice show complete loss of endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187 (J:54772)
• in contrast, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are enhanced resulting in a shift of EC50 by ~7-fold relative to wild-type values (J:54772)
• homozygotes display mild bradycardia relative to wild-type mice (J:54772)
• notably, chronic treatment of homozygotes with L-NAME induces a significant decrease of heart rate in both wild-type mice and mutant mice (J:54772)
• homozygotes display mild bradycardia relative to wild-type mice (J:54772)
• notably, chronic treatment of homozygotes with L-NAME induces a significant decrease of heart rate in both wild-type mice and mutant mice (J:54772)
• increase in blood pressure by about 18 mmHg (J:36559)
• increase in blood pressure by about 18 mmHg (J:36559)
• homozygotes exhibit modest hypertension relative to wild-type mice (J:54772)
• chronic treatment of homozygotes with NOS inhibitor L-NAME fails to further increase blood pressure; in contrast, chronic L-NAME treatment increases blood pressure in wild-type (C57BL/6J) mice to a level similar to that noted in mutant mice (J:54772)
• homozygotes exhibit modest hypertension relative to wild-type mice (J:54772)
• chronic treatment of homozygotes with NOS inhibitor L-NAME fails to further increase blood pressure; in contrast, chronic L-NAME treatment increases blood pressure in wild-type (C57BL/6J) mice to a level similar to that noted in mutant mice (J:54772)

growth/size/body
• body weight is approximately 7.5% lower than wild-type at 14 weeks of age (J:36559)
• body weight is approximately 7.5% lower than wild-type at 14 weeks of age (J:36559)

homeostasis/metabolism
N
• unlike mice null for Nos1 or Nos2, no abnormalities in urine pH or bicarbonate concentrations are detected (J:64896)
• unlike mice null for Nos1 or Nos2, no abnormalities in urine pH or bicarbonate concentrations are detected (J:64896)
• plasma renin is nearly 2x that of wild-type (J:36559)
• plasma renin is nearly 2x that of wild-type (J:36559)

muscle
• aortic rings isolated from homozygous mutant mice exhibit a significantly enhanced vasoconstriction in response to phenylephrine and a modestly enhanced vasoconstriction in response to serotonin (J:54772)
• aortic rings isolated from homozygous mutant mice exhibit a significantly enhanced vasoconstriction in response to phenylephrine and a modestly enhanced vasoconstriction in response to serotonin (J:54772)
• aortic rings isolated from homozygous mutant mice show complete loss of endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187 (J:54772)
• in contrast, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are enhanced resulting in a shift of EC50 by ~7-fold relative to wild-type values (J:54772)
• aortic rings isolated from homozygous mutant mice show complete loss of endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187 (J:54772)
• in contrast, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are enhanced resulting in a shift of EC50 by ~7-fold relative to wild-type values (J:54772)




Genotype
MGI:5427346
ht7
Allelic
Composition
Nos3tm1Unc/Nos3+
Genetic
Background
B6.129P2-Nos3tm1Unc/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 38% of mice die by P10 compared with 13% of wild-type mice (J:103270)
• 38% of mice die by P10 compared with 13% of wild-type mice (J:103270)




Genotype
MGI:3630165
ht8
Allelic
Composition
Nos3tm1Unc/Nos3+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• aortic rings isolated from normotensive heterozygous mutant mice show normal endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187 (J:54772)
• however, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are modestly enhanced in heterozygous aortic rings relative to wild-type (J:54772)
• aortic rings isolated from normotensive heterozygous mutant mice show normal endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187 (J:54772)
• however, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are modestly enhanced in heterozygous aortic rings relative to wild-type (J:54772)

muscle
• aortic rings isolated from normotensive heterozygous mutant mice show normal endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187 (J:54772)
• however, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are modestly enhanced in heterozygous aortic rings relative to wild-type (J:54772)
• aortic rings isolated from normotensive heterozygous mutant mice show normal endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187 (J:54772)
• however, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are modestly enhanced in heterozygous aortic rings relative to wild-type (J:54772)




Genotype
MGI:3794764
cx9
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
B6.129P2-Nos3tm1Unc Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• microaneurysmal dilations in 20% of males (J:60670)
• sometimes involving coronary arteries (J:60670)
• microaneurysmal dilations in 20% of males (J:60670)
• sometimes involving coronary arteries (J:60670)
• plaques larger at 4 months than in Apoe homozygotes, by 182% for males and 165% for females (J:60670)
• plaques larger at 4 months than in Apoe homozygotes, by 182% for males and 165% for females (J:60670)
• plaques in descending aorta in 90% of males as opposed to 20% of Apoe males (J:60670)
• plaques in descending aorta in 90% of males as opposed to 20% of Apoe males (J:60670)
• about 20mm higher than in Apoe homozygotes (J:60670)
• about 20mm higher than in Apoe homozygotes (J:60670)

renal/urinary system
• 15% of glomeruli with large lipid deposits in foam cells filling the glomeruli (J:60670)
• glomerular injury progresses to dystrophic calcification and glomerular loss (J:60670)
• 15% of glomeruli with large lipid deposits in foam cells filling the glomeruli (J:60670)
• glomerular injury progresses to dystrophic calcification and glomerular loss (J:60670)
• 15% lower than in Apoe homozygotes (J:60670)
• 15% lower than in Apoe homozygotes (J:60670)

homeostasis/metabolism
• 66% higher than controls (J:60670)
• 66% higher than controls (J:60670)




Genotype
MGI:4367219
cx10
Allelic
Composition
Nos2tm1Lau/Nos2tm1Lau
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
B6.129P2-Nos3tm1Unc Nos2tm1Lau
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos2tm1Lau mutation (6 available); any Nos2 mutation (12 available)
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• fewer than expected double homozygotes are born, no time of lethality provided (J:83112)
• fewer than expected double homozygotes are born, no time of lethality provided (J:83112)




Genotype
MGI:4361710
cx11
Allelic
Composition
Leprdb/Leprdb
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
BKS.Cg-Leprdb Nos3tm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Leprdb mutation (11 available); any Lepr mutation (37 available)
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• albumin/creatinine ratio (ACR) is significantly higher than all controls (J:135864)
• albumin/creatinine ratio (ACR) is significantly higher than all controls (J:135864)
• arteriolar hyalinosis (J:135864)
• arteriolar hyalinosis (J:135864)
• glomerular basement membrane is markedly thickened by 16 weeks in comparison to all controls (J:135864)
• glomerular basement membrane is markedly thickened by 16 weeks in comparison to all controls (J:135864)
• glomerular injury is significantly increased by 24-26 weeks in comparison to all controls (J:135864)
• glomerular injury is significantly increased by 24-26 weeks in comparison to all controls (J:135864)
• marked mesangial expansion is observed at 26 weeks of age (J:135864)
• marked mesangial expansion is observed at 26 weeks of age (J:135864)
• marked mesangiolysis is observed at 26 weeks of age (J:135864)
• marked mesangiolysis is observed at 26 weeks of age (J:135864)
• focal nodular sclerosis is observed at 26 weeks of age (J:135864)
• focal nodular sclerosis is observed at 26 weeks of age (J:135864)
• substantial fibronectin accumulation is observed in glomeruli (J:135864)
• substantial fibronectin accumulation is observed in glomeruli (J:135864)
• GFR is decreased in comparison to homozygous Nos3tm1Unc and Leprdb controls (J:135864)
• GFR is decreased in comparison to homozygous Nos3tm1Unc and Leprdb controls (J:135864)

homeostasis/metabolism
• at 26 weeks, serum creatinine is significantly higher than all controls (J:135864)
• at 26 weeks, serum creatinine is significantly higher than all controls (J:135864)
• hyperglycemia is first observed between 6-8 weeks of age, but is not higher than homozygous Leprdb control (J:135864)
• hyperglycemia is first observed between 6-8 weeks of age, but is not higher than homozygous Leprdb control (J:135864)
• albumin/creatinine ratio (ACR) is significantly higher than all controls (J:135864)
• albumin/creatinine ratio (ACR) is significantly higher than all controls (J:135864)

growth/size/body
• at 26 weeks, body weight is double that of lean and Nos3tm1Unc controls (J:135864)
• at 26 weeks, body weight is double that of lean and Nos3tm1Unc controls (J:135864)

cardiovascular system
• arteriolar hyalinosis (J:135864)
• arteriolar hyalinosis (J:135864)
• hypertension is observed between 24-28 weeks of age, but is not significantly higher than homozygous Nos3tm1Unc controls (J:135864)
• hypertension is observed between 24-28 weeks of age, but is not significantly higher than homozygous Nos3tm1Unc controls (J:135864)

Mouse Models of Human Disease
OMIM ID Ref(s)
Diabetes Mellitus, Noninsulin-Dependent; NIDDM 125853 J:135864




Genotype
MGI:4367218
cx12
Allelic
Composition
Nos1tm1Plh/Nos1tm1Plh
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos1tm1Plh mutation (3 available); any Nos1 mutation (11 available)
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• fewer than expected double homozygotes are born, no time of lethality provided (J:83112)
• fewer than expected double homozygotes are born, no time of lethality provided (J:83112)





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
Citing These Resources
Funding Information
Warranty Disclaimer & Copyright Notice
Send questions and comments to User Support.
last database update
02/02/2016
MGI 6.02
The Jackson Laboratory