Phenotypes Associated with This Genotype

Genotype
MGI:3621887

• Allelic Composition: Apoe^tm1Unc/Apoe^tm1Unc; Cst3^tm1Karl/Cst3^tm1Karl
• Genetic Background: involves: 129S/SvEv * C57BL/6

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

homeostasis/metabolism

abnormal enzyme/coenzyme level ( J:106879 )

• aortic tissue extracts from double knockouts show higher levels of cathepsins S and L and the long form of cathepsin B than ApoE null controls

abnormal enzyme/coenzyme activity ( J:106879 )

• aortic smooth muscle cells exhibit an augmented ability to degrade elastin in vitro

cardiovascular system

abnormal aorta tunica media morphology ( J:106879 )

• double knockout mice display thinning of the tunica media in the aortic arch compared to ApoE knockouts

abnormal aorta elastic tissue morphology ( J:106879 )

• double knockouts show more framentation of elastic laminae than in either the ApoE or Cst3 single knockout mouse

abnormal aortic arch morphology ( J:106879 )

• double knockout mice display thinning of the tunica media in the aortic arch compared to ApoE knockouts

atherosclerotic lesions ( J:106879 )

• atherosclerotic lesions from aortas of double knockouts had increased smooth muscle cell content (9.3% vs. 4.2% positive lesion area) and collagen (14.4% vs. 4.6%) compared to ApoE knockout mice; fibrous caps develop significantly more in double mutants than controls

vascular smooth muscle hyperplasia ( J:106879 )

• in vitro double knockout smooth muscle cells proliferate more rapidly than control cells which might contribute to the increase in SMC and collagen content in aortic lesions

muscle

vascular smooth muscle hyperplasia ( J:106879 )

• in vitro double knockout smooth muscle cells proliferate more rapidly than control cells which might contribute to the increase in SMC and collagen content in aortic lesions