Bone marrow endothelial progenitors augment atherosclerotic plaque regression in a mouse model of plasma lipid lowering.

ABSTRACT: The major event initiating atherosclerosis is hypercholesterolemia-induced disruption of vascular endothelium integrity. In settings of endothelial damage, endothelial progenitor cells (EPCs) are mobilized from bone marrow into circulation and home to sites of vascular injury where they aid endothelial regeneration. Given the beneficial effects of EPCs in vascular repair, we hypothesized that these cells play a pivotal role in atherosclerosis regression. We tested our hypothesis in the atherosclerosis-prone mouse model in which hypercholesterolemia, one of the main factors affecting EPC homeostasis, is reversible (Reversa mice). In these mice, normalization of plasma lipids decreased atherosclerotic burden; however, plaque regression was incomplete. To explore whether endothelial progenito

SUBMITTER: Yao L 

PROVIDER: S-EPMC3508339 | biostudies-literature | 2012 Dec

REPOSITORIES: biostudies-literature