Targeted mouse complement inhibitor CR2-Crry protects against the development of atherosclerosis in mice.

ABSTRACT:

Objective

Atherosclerosis is a chronic inflammatory and immune vascular disease, and clinical and experimental evidence has indicated an important role of complement activation products, including the terminal membrane attack complex (MAC), in atherogenesis. Here, we investigated whether complement inhibition represents a potential therapeutic strategy to treat/prevent atherogenesis using CR2-Crry, a recently described complement inhibitor that specifically targets to sites of C3 activation.

Methods and results

Previous studies demonstrated that loss of CD59 (a membrane inhibitor of MAC formation) accelerated atherogenesis in Apoe deficient (Apoe(-/-)) mice. Here, both CD59 sufficient and CD59 deficient mice in an Apoe deficient background (namely, mCd59 ab(+/+)/Apoe(-/-) an

SUBMITTER: Liu F 

PROVIDER: S-EPMC4267679 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature