Disruption of SEMA4D ameliorates platelet hypersensitivity in dyslipidemia and confers protection against the development of atherosclerosis.

ABSTRACT:

Objective

In dyslipidemic states, platelets become hyperreactive, secreting molecules that promote atherosclerosis. We have shown that the semaphorin family member, sema4D (CD100), is expressed on the surface of platelets and proposed that its role includes promoting thrombus growth by binding to nearby platelets and endothelial cells, both of which express sema4D receptors. Here we tested the hypothesis that deleting sema4D will attenuate the adverse consequences of dyslipidemia on platelets and the vessel wall.

Methods and results

Platelet function and atherosclerotic lesion formation were measured in LDLR(-/-) and sema4D(-/-)LDLR(-/-) mice after 6 months on a high-fat diet. All of the mice developed the dyslipidemia expected on this diet in the absence of functional LDL r

SUBMITTER: Zhu L 

PROVIDER: S-EPMC2877695 | biostudies-literature | 2009 Jul

REPOSITORIES: biostudies-literature