AimTo investigate the effect of C-reactive protein (CRP)on rat bone marrow-derived endothelial progenitor cells (EPC)involved into vasculogenesis and functional activity in vitro, and discuss possible mechanism of CRP during progression of atherosclerosis.MethodsEPC were separated from bone marrow of rat with density gradient centrifugation, and characterized as DiI-ac-LDL/FITC-UEA-l double positive cells detected by laser confocal microscopy.EPC were cultured with CRP of different concentrations (0， 1, 5 and 10 mg/L) for 24 h.A co-culture model of EPC and rat cardiac microvascular endothelial cells (CMEC) was used to analyze the effect of CRP on EPC involved into lumen formation in vitro.Proliferation viability, migration, vasculogenesis, and protein expression of EPC were assayed by MTT, Transwell chamber, Matrigel, Western blotting respectively.ResultsCRP dose-dependently reduced the number of EPC involved into capillary-like structures of CMEC, weakened proliferation viability of EPC, reduced the number of migration and lumen formation, up-regulated the expression of Bax protein, and down-regulated the expression of Bcl-2 protein, integrin β2, endogenous vescular endothelial growth factor (VEGF).ConclusionCRP may impair EPC-mediated neovascularization by weakening its functions, which leads to progression of atherosclerosis.