Chen YangXin, Wang JingFeng, Yao YouJie, Yuan WoLiang, Kong MinYi, Lin YongQing, Geng DengFeng, Nie RuQiong
Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China.
FEBS Lett. 2009 Sep 3;583(17):2811-8. doi: 10.1016/j.febslet.2009.07.037. Epub 2009 Jul 23.
It was found that C-reactive protein (CRP) could significantly increase the expression and activity of tissue factor (TF), but decrease that of tissue factor pathway inhibitor (TFPI) in human umbilical vein endothelial cells (HUVECs) in dose- and time-dependent manners, which could be antagonized by PDTC and U0126. CRP could also increase protein expression of phosphorylated nuclear factor-kappaB (NF-kappaB), IkappaB-alpha and ERK1/2 in dose- and time-dependent manner. In addition, neutralizing antibody to CD32 (FcgammaR II) could significantly attenuate the expression and activity of TF and TFPI induced by CRP. These results suggest that CRP may promote coagulation by enhancing the expression and activity of TF and reducing that of TFPI by activating NF-kappaB and extracellular signal-regulated kinase via FcgammaR II.
研究发现，C反应蛋白（CRP）可呈剂量和时间依赖性地显著增加人脐静脉内皮细胞（HUVECs）中组织因子（TF）的表达和活性，但降低组织因子途径抑制物（TFPI）的表达和活性，而这一作用可被PDTC和U0126拮抗。CRP还可呈剂量和时间依赖性地增加磷酸化核因子-κB（NF-κB）、IκB-α和ERK1/2的蛋白表达。此外，CD32（FcγR II）中和抗体可显著减弱CRP诱导的TF和TFPI的表达及活性。这些结果表明，CRP可能通过FcγR II激活NF-κB和细胞外信号调节激酶，增强TF表达和活性、降低TFPI表达和活性，从而促进凝血。
