C-reactive protein can influence the proliferation, apoptosis, and monocyte chemotactic protein-1 production of human umbilical vein endothelial cells.

C-reactive protein (CRP) has been shown to be closely associated with coronary heart disease. The serum CRP concentrations of chronic periodontitis (CP) patients were increased due to periodontal inflammation. CRP may be a potential key mediator associating CP with coronary heart disease. This study aimed to investigate the effects of CRP on human endothelial cells in vitro. CRP ranging from 0 to 10 μg/mL was adopted to imitate the chronic inflammatory conditions of periodontitis. The influences of CRP on proliferation, apoptosis, and monocyte chemotactic protein-1 (MCP-1) production of human umbilical vein endothelial cells (HUVECs) were studied through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, and enzyme-linked immunosorbent assay analysis, respectively. Compared to the blank control, 2.5 and 5.0 μg/mL CRP significantly suppressed cell proliferation by 6.9% and increased apoptosis by 10.2% and 14.6%, respectively (p<0.05). Concentrations of 7.5 and 10.0 μg/mL CRP also induced 2.3% HUVEC proliferation suppression (p>0.05) and significantly increased apoptosis ratio compared to that of the blank control. CRP could promote MCP-1 production of HUVECs in a concentration-dependent manner. The MCP-1 production of 10.0 μg/mL CRP group was about 15.3% higher than that of the control group. It is concluded that low concentrations of CRP, which appears in CP, inhibits cell proliferation, promotes cell apoptosis, and increases MCP-1 production in endothelium, which may initiate self-repairing function of vascular endothelium following vascular injury process.