C-reactive protein induced inflammatory response in pulmonary artery smooth muscle cell by nuclear factor-κB pathway
10.3760/cma.j.issn.1671-0282.2011.04.013
- VernacularTitle: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
- Author:
Ling HOU
;
Jinke ZHOU
;
Jie LI
;
Hua ZHENG
;
Changlin LU
- Publication Type:Journal Article
- Keywords:
Pulmonary artery smooth muscle cells;
C-reactive protein;
Inflammation;
FcγⅡa receptor;
Nuclear factor κB;
Interleukin -6;
Pulmonary artery hypertension
- From:
Chinese Journal of Emergency Medicine
2011;20(4):395-399
- CountryChina
- Language:Chinese
-
Abstract:
Objective To examine the impact of C-reactive protein (CRP) on the expression of interleukin-6 (IL-6), inflammatory cytokine, in cultured human pulmonary artery smooth muscle cells (hPASMCs) in order to find out the cause of pulmonary artery hypertension (PAH). Method The hPASMCs were cultured and stimulated by different concerntrations of CRP (5 - 200 μg/ml) for different lengths of time. The activity of nuclear factor-κB (NF-κB) was evaluated by electrophoretic gel mobility shift assay (EMSA). The expression of IL-6 mRNA and the level of IL-6 protein were measured by using real-time PCR and ELISA, respectively. Results CRP increased IL-6 production in hPASMCs in a dose-dependent manner. The increase in IL-6 at concerntration of 200 μg/mL in the CRP group was as high as 2.8times that in the control group. CRP also significantly induced the activation of NF-κB in hPASMCs. The effect of CRP on the inflammatory cytokine, IL-6, was inhibited by the specific FcγⅡa receptor antibody.Conclusions In vitro, CRP increases the production of IL-6 in hPASMCs mediated by FcγⅡa receptor and NF-κB translocation. These data offer important insights into the role of CRP in the pathogenesis of PAH.
