ApoER2 (Apolipoprotein E Receptor-2) Deficiency Accelerates Smooth Muscle Cell Senescence via Cytokinesis Impairment and Promotes Fibrotic Neointima After Vascular Injury.

ABSTRACT:

Objective

Genome-wide studies showed that mutation in apoER2 (apolipoprotein E receptor-2) is additive with ε4 polymorphism in the APOE gene on cardiovascular disease risk in humans. ApoE or apoER2 deficiency also accelerates atherosclerosis lesion necrosis in hypercholesterolemic mice and promotes neointima formation after vascular injury. This study tests the hypothesis that apoE and apoER2 modulate vascular occlusive diseases through distinct mechanisms. Approach and Results: Carotid endothelial denudation induced robust neointima formation in both apoE^-/- and apoER2-deficient Lrp8^-/- mice. The intima in apoE^-/- mice was rich in smooth muscle cells, but the intima in Lrp8^-/- mice was cell-poor and ric

SUBMITTER: Komaravolu RK 

PROVIDER: S-EPMC6761011 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature