B6.129P2-Apoe^tm1Unc/J 

002052

• One of the most relevant models for atherosclerosis research
• Hypercholesterolemic and spontaneously develop arterial lesions
• Atherosclerosis progression very similar to that in humans
• By 3 months, homozygotes develop fatty streaks in the proximal aorta
• Develop lesions more quickly if fed a Western diet (containing 21% fat and 0.15% cholesterol), and even more quickly if fed a high-cholesterol diet (containing 15% fat, 1.25% cholesterol, and 0.5% cholic acid)
• With age, develop more lesions with relatively less lipid but more elongated cells, typical of the advanced stage pre-atherosclerotic lesions (Jawien et al. 2004)
• Extensive phenotypic data available from the Mouse Phenome Database

B6.129S7-Ldlr^tm1Her/J 

002207

• High serum cholesterol levels (200-400 mg/dl) on regular chow diet
• Very high levels (> 2,000 mg/dl) when fed a high fat diet (normal levels are 80-100 mg/dl)
• Develop small atherosclerotic lesions spontaneously but slowly when fed chow
• Lesions develop much faster when fed either high cholesterol or Western diet (Jawien et al. 2004)

C57BL/6J 

000664

• Highly susceptible to diet-induced atherosclerosis: after feeding an atherogenic diet (15% fat, 1.25% cholesterol and 0.5% sodium cholate) for 12 weeks, both young and old mice develop moderate hypercholesterolemia and form fatty streaks at the aortic root (Li et al. 2008)
• Highly susceptible to diet-induced obesity
• The most widely used, best characterized, and only fully sequenced inbred mouse strain
• Part of our unique Genetic Stability Program, which effectively stops cumulative genetic drift
• Extensive phenotypic data available from the Mouse Phenome Database

C57L/J 

000668

• Highly susceptible to diet-induced atherosclerosis: after feeding an atherogenic diet (15% fat, 1.25% cholesterol and 0.5% sodium cholate) mice develop atherosclerotic aortic lesions (Paigen et al. 1990)
• Susceptible to diet-induced gallstones (Xu et al. 2004)
• Extensive phenotypic data available from the Mouse Phenome Database

SM/J 

000687

• Highly susceptible to diet-induced atherosclerosis: after feeding an atherogenic diet (15% fat, 1.25% cholesterol and 0.5% sodium cholate) mice develop atherosclerotic aortic lesions (Paigen et al. 1990)
• Susceptible to diet-induced obesity
• Extensive phenotypic data available from the Mouse Phenome Database

C57BL/6-Tg(APOA1)1Rub/J 

001927

• High concentration of APOA1 in the artery wall likely enhances cellular cholesterol efflux and protects against atherosclerosis
• Homozygotes viable, fertile, and normal-sized
• Twice as much total plasma cholesterol but over four times less mouse APOAI than normal
• Resistant to diet-induced fatty streak lesions (Rubin et al. 1991)

B6.129P2-Apoa1^tm1Unc/J 

002055

• Homozygotes appear to develop normally despite having no APOA1 protein
• After being fasted overnight, exhibit severely reduced levels of plasma cholesterol and HDL-cholesterol
• Deficient in alpha-migrating HDL particles (Williamson et al. 1992)
• Cholesterol absorption slow and significantly reduced (Iqbal and Hussain 2005)

 

B6.129P2-Nos3^tm1Unc/J 

002684

• Blood pressure approximately 20 mmHg higher than that of normal wild-type siblings
• Low heart rate (Bradycardia)
• Insulin resistant in the liver and peripheral tissues (Shesely et al. 1996)

BPH/2J, BPL/1J, BPN/3J 

003005, 003006, 003004

• Descendants from an 8-way cross from which hypertensive and hypotensive mouse lines were selected (Schlager and Sides 1997)
• BPH/2J is hypertensive: by 5 weeks, has high systolic blood pressures; by 150 days, blood pressure is 60mmHg higher than BPL/1J; higher heart rate, larger hearts and kidneys, and higher hematocrit counts than BPL/1J; lower renin, aldosterone, and angiotensin levels than BPL/1J and BPN/3J
• BPL/1J is hypotensive
• BPN/3J is normotensive: inbred at the same time as and from the same parental strain as BPL/1J and BPN/3J, but in the absence of any selection pressure; normotensive control for BPH/2J and BPL/1J
• 3-5 genes likely responsible for the difference in blood pressures between BPH/2 and BPL/1 mice (Schlager and Sides 1997; Uddin and Harris-Nelson 2004)
• Observations by JAX scientists (Paigen and Svenson, pers. comm.) suggest that BPH/2J may be a model of preeclampsia: appears to have several preeclampsia phenotypes, including small litters of 1-2 pups (Dokras et al. 2006; Davisson et al. 2002)
• Phenotypic data for BPH/2J, BPL/1J, and BPN/3J available from the Mouse Phenome Database

129S/SvEv-Tg(Alb1-Ren)1Unc/CofJ

007853

• Hemizygotes have very high blood pressure, polydipsia, polyuria, proteinuria, and kidney damage
• Cardiac hypertrophy with fibrosis and 50% male mortality between 6-8 months, due to increased circulating levels of angiotensin II High ectopic levels of active mouse renin in the liver and high plasma levels of prorenin and active renin
• May be used to study the effects of genetically clamped renin (and angiotensin II) on hypertension, diabetic nephropathy, albuninurea, nephrosclerosis, and other cardiovascular disorders (Caron et al. 2002, 2004)

B6.129P2-Nos3^tm1Unc/J 

002684

• Low heart rate (Bradycardia)
• Blood pressure approximately 20 mmHg higher than that of normal wild-type siblings
• Insulin resistant in the liver and peripheral tissues (Shesely et al. 1996)

129S/SvEv-Tg(Alb1-Ren)1Unc/CofJ 

007853

• Hemizygotes have very high blood pressure, polydipsia, polyuria, proteinuria, and kidney damage
• Cardiac hypertrophy with fibrosis and 50% male mortality between 6-8 months, due to increased circulating levels of angiotensin II
• High ectopic levels of active mouse renin in the liver and high plasma levels of prorenin and active renin
• May be used to study the effects of genetically clamped renin (and angiotensin II) on hypertension, diabetic nephropathy, albuninurea, nephrosclerosis, and other cardiovascular disorders (Caron et al. 2002, 2004)

B6.129-Fbn1^tm1Hcd/J 

012885

• Cys1039Tyr mutation is similar to the human mutation that underlies classic Marfan syndrome
• Heterozygotes develop proximal aortic aneurysms, mitral valve thickenings, pulmonary alveolar septation defects, mild thoracic kyphosis, and skeletal myopathy

• Most heterozygotes (90%) live to one year of age