RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis.

ABSTRACT:

Objective

The objective of this study is to determine the role and underlying mechanisms of RGC-32 (response gene to complement 32 protein) in atherogenesis.

Approach and results

RGC-32 was mainly expressed in endothelial cells of atherosclerotic lesions in both ApoE^-/- (apolipoprotein E deficient) mice and human patients. Rgc-32 deficiency (Rgc32^-/-) attenuated the high-fat diet-induced and spontaneously developed atherosclerotic lesions in ApoE^-/- mice without affecting serum cholesterol concentration. Rgc32^-/- seemed to decrease the macrophage content without altering collagen and smooth muscle contents or lesional macrophage proliferation in the lesions. Transplantation of WT (wild type) mouse bone marrow t

SUBMITTER: Cui XB 

PROVIDER: S-EPMC5864544 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature