核因子κB途径介导C反应蛋白对肺动脉平滑肌细胞的促炎作用

Abstract

：Objective To examine theimpact of C-reactive protein (CRP) on the expression of interleukin-6 (IL-6), inflammatorycytokine, in cultured human pulmonary artery smooth muscle cells (hPASMCs) in order tofind out the cause of pulmonary artery hypertension (PAH). Method The hPASMCs werecultured and stimulated by different concerntrations of CRP (5 - 200 μg/ml) for different lengths of time. The activity ofnuclear factor-κB (NF-κB) was evaluated byelectrophoretic gel mobility shift assay (EMSA). The expression of IL-6 mRNA and the levelof IL-6 protein were measured by using real-time PCR and ELISA, respectively. Results CRPincreased IL-6 production in hPASMCs in a dose-dependent manner. The increase in IL-6 atconcerntration of 200 μg/mLin the CRP group was as high as 2.8times that in the control group. CRP also significantlyinduced the activation of NF-κB in hPASMCs. The effect of CRP on the inflammatory cytokine, IL-6, was inhibitedby the specific FcγⅡareceptor antibody.Conclusions In vitro, CRP increases the production of IL-6 in hPASMCsmediated by FcγⅡareceptor and NF-κBtranslocation. These data offer important insights into the role of CRP in thepathogenesis of PAH. Key words: Pulmonary artery smooth muscle cells; C-reactive protein; Inflammation; Fc