作者: Florin Niculescu , Tudor Badea , Horea Rus
DOI: 10.1016/S0021-9150(98)00185-3
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摘要: Proliferation of vascular smooth muscle cells contributes to initimal hyperplasia during atherogenesis, but the factors regulating their proliferation are not well known. In present study we report that sublytic C5b-9 assembly induced differentiated human aortic (ASMC) in culture. Cell cycle re-entry occurred through activation cdk4, cdk2 kinase and reduction p21 cell inhibitor. We also investigated if induction is mediated mitogen activated protein (MAPK) pathways. Extracellular signal regulated (ERK) 1 activity was significantly increased, while c-jun NH2-terminal (JNK) p38 MAPK were only transiently increased. Pretreatment with wortmannin inhibits ERK1 by C5b-9, suggesting involvement phosphatidylinositol 3-kinase (PI 3-kinase). Both PI p70 S6 C5b6. DNA synthesis abolished pretreatment inhibitors 3-kinase, MAPK. These data indicated play a major role ASMC proliferation.