C-Reactive Protein Induces Interleukin-6 and Thrombospondin-1 Protein and mRNA Expression through Activation of Nuclear Factor-kappa B in HK-2 Cells
文献类型：期刊论文
| 作者 | Wang, Hai-rong1; Chen, De-liang1; Zhao, Mingming1; Shu, Shao-wu2; Xiong, Shi-xi1; Gan, Xue-dong1; Chao, Sheng-ping1; Cao, Jian-lei1 |
| 刊名 | KIDNEY & BLOOD PRESSURE RESEARCH
 |
| 出版日期 | 2012 |
| 卷号 | 35期号:4页码:211-219 |
| 关键词 | C-reactive protein Renal tubular epithelial cells Mitogen-activated protein kinase Nuclear factor-kappa B Interleukin-6 Thrombospondin-1 |
| ISSN号 | 1420-4096 |
| 通讯作者 | Wang, HR (reprint author), Wuhan Univ, Zhongnan Hosp, Dept Cardiol, 169 Dong Hu Rd, Wuhan 430071, Peoples R China. |
| 中文摘要 | Background: Although C-reactive protein (CRP) is significantly increased in patients with diabetic nephropathy, whether CRP exerts direct proinflammatory effects on human renal tubular epithelial cells (HK-2 cells) is still unclear. Methods: HK-2 cells were incubated with purified CRP at clinically relevant concentrations (0, 5, 10, 20 and 40 mu g/ml). The protein and transcript levels of thrombospondin-1 (TSP-1) and interleukin-6 (IL-6) were determined by ELISA and RT-PCR. Phosphorylation of p38MAPK was investigated through Western blot analysis in HK-2 cells induced by CRP. The activation of nuclear factor-kappa B (NF-kappa B) was studied via EMSA. A specific p38MAPK inhibitor (SB203580) and an NF-kappa B inhibitor (PDTC; pyrrolidine dithiocarbamate) were used to analyze the signal transduction in CRP induction. To explore the direct or indirect role of CRP in HK-2 cells, IL-6 or TSP-1 antibodies were used. The expression of IL-6, TSP-1 and transforming growth factor-beta(1) (TGF-beta(1)) were determined through Western blot analysis in HK-2 cells. Results: In HK-2 cells, purified CRP significantly induced protein release and mRNA expression of IL-6 and TSP-1 in a dose- and time-dependent manner. TGF-beta(1) protein was overexpressed in HK-2 cells induced by CRP, which cannot be inhibited by IL-6 or TSP-1 antibodies. CRP triggered phosphorylation of p38MAPK and activation of NF-kappa B-mediated signal transduction. SB203580 (5 mu m) and PDTC (50 mu m) efficiently suppressed those effects of CRP in HK-2 cells. Conclusions: CRP induces IL-6 and TSP-1 protein release and mRNA expression from HK-2 cells via activation of the p38MAPK and NF-kappa B signaling pathways and TGE-beta(1) was highly expressed in HK-2 cells, suggesting that CRP plays an important role in the propagation and prolongation of inflammation in renal fibrosis. Copyright (C) 2012 S. Karger AG, Basel |
| 英文摘要 | Background: Although C-reactive protein (CRP) is significantly increased in patients with diabetic nephropathy, whether CRP exerts direct proinflammatory effects on human renal tubular epithelial cells (HK-2 cells) is still unclear. Methods: HK-2 cells were incubated with purified CRP at clinically relevant concentrations (0, 5, 10, 20 and 40 mu g/ml). The protein and transcript levels of thrombospondin-1 (TSP-1) and interleukin-6 (IL-6) were determined by ELISA and RT-PCR. Phosphorylation of p38MAPK was investigated through Western blot analysis in HK-2 cells induced by CRP. The activation of nuclear factor-kappa B (NF-kappa B) was studied via EMSA. A specific p38MAPK inhibitor (SB203580) and an NF-kappa B inhibitor (PDTC; pyrrolidine dithiocarbamate) were used to analyze the signal transduction in CRP induction. To explore the direct or indirect role of CRP in HK-2 cells, IL-6 or TSP-1 antibodies were used. The expression of IL-6, TSP-1 and transforming growth factor-beta(1) (TGF-beta(1)) were determined through Western blot analysis in HK-2 cells. Results: In HK-2 cells, purified CRP significantly induced protein release and mRNA expression of IL-6 and TSP-1 in a dose- and time-dependent manner. TGF-beta(1) protein was overexpressed in HK-2 cells induced by CRP, which cannot be inhibited by IL-6 or TSP-1 antibodies. CRP triggered phosphorylation of p38MAPK and activation of NF-kappa B-mediated signal transduction. SB203580 (5 mu m) and PDTC (50 mu m) efficiently suppressed those effects of CRP in HK-2 cells. Conclusions: CRP induces IL-6 and TSP-1 protein release and mRNA expression from HK-2 cells via activation of the p38MAPK and NF-kappa B signaling pathways and TGE-beta(1) was highly expressed in HK-2 cells, suggesting that CRP plays an important role in the propagation and prolongation of inflammation in renal fibrosis. Copyright (C) 2012 S. Karger AG, Basel |
| WOS标题词 | Science & Technology ; Life Sciences & Biomedicine |
| 类目[WOS] | Physiology ; Urology & Nephrology ; Peripheral Vascular Disease |
| 研究领域[WOS] | Physiology ; Urology & Nephrology ; Cardiovascular System & Cardiology |
| 关键词[WOS] | TUMOR-NECROSIS-FACTOR ; SMOOTH-MUSCLE-CELLS ; IN-VITRO ; CARDIOVASCULAR-DISEASE ; ENDOTHELIAL-CELLS ; TNF-ALPHA ; INFLAMMATION ; MACROPHAGES ; INHIBITION ; GAMMA |
| 收录类别 | SCI |
| 资助信息 | Hubei Province Scientific Research Foundation[2007AA301B36-3, 2009CDB059]; Hubei Province Health Department Important Foundation[JX2A19]; State Key Laboratory of Freshwater Ecology and Biotechnology[2010FB12] |
| 语种 | 英语 |
| WOS记录号 | WOS:000303846100002 |
| 公开日期 | 2012-09-25 |
| 源URL | [http://ir.ihb.ac.cn/handle/342005/16961]  |
| 专题 | 水生生物研究所_鱼类生物学及渔业生物技术研究中心_期刊论文 |
| 作者单位 | 1.Wuhan Univ, Zhongnan Hosp, Dept Cardiol, Wuhan 430071, Peoples R China 2.State Key Lab Freshwater Ecol & Biotechnol, Wuhan, Peoples R China |
| 推荐引用方式 GB/T 7714 | Wang, Hai-rong,Chen, De-liang,Zhao, Mingming,et al. C-Reactive Protein Induces Interleukin-6 and Thrombospondin-1 Protein and mRNA Expression through Activation of Nuclear Factor-kappa B in HK-2 Cells[J]. KIDNEY & BLOOD PRESSURE RESEARCH,2012,35(4):211-219. |
| APA | Wang, Hai-rong.,Chen, De-liang.,Zhao, Mingming.,Shu, Shao-wu.,Xiong, Shi-xi.,...&Cao, Jian-lei.(2012).C-Reactive Protein Induces Interleukin-6 and Thrombospondin-1 Protein and mRNA Expression through Activation of Nuclear Factor-kappa B in HK-2 Cells.KIDNEY & BLOOD PRESSURE RESEARCH,35(4),211-219. |
| MLA | Wang, Hai-rong,et al."C-Reactive Protein Induces Interleukin-6 and Thrombospondin-1 Protein and mRNA Expression through Activation of Nuclear Factor-kappa B in HK-2 Cells".KIDNEY & BLOOD PRESSURE RESEARCH 35.4(2012):211-219. |
入库方式： OAI收割
来源：水生生物研究所
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