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p~(38)MAPK在IL-18诱导肾小管上皮细胞转分化中的作用
引用本文:张军峰,姚翠微,刘华锋,梁东,陈孝文. p~(38)MAPK在IL-18诱导肾小管上皮细胞转分化中的作用[J]. 中国应用生理学杂志, 2010, 0(2): 199-201
作者姓名:张军峰  姚翠微  刘华锋  梁东  陈孝文
作者单位:广东医学院附属医院肾病研究所,湛江524001
基金项目:广东省自然科学基金资助(5011589)
摘    要:目的:白细胞介素18(IL-18)可诱导肾小管上皮细胞转分化,本研究探讨其是否是通过p38MAPK途径而起作用。方法:应用不同浓度的p38MAPK通路特异性阻断剂SB203580(0、5、10、20μmol/L)预孵育人近端肾小管上皮细胞(HK-2细胞)30min后,加入IL-18(100ng/ml)共培养24、48、72h。应用RT-PCR法检测α-平滑肌肌动蛋白(α-SMA)mRNA的表达水平;应用ELISA法测定细胞浆中α-SMA蛋白质含量。结果:SB203580呈剂量依赖性地抑制IL-18诱导的HK-2细胞α-SMA基因表达(P0.05)。结论:p38MAPK通路是调控IL-18诱导肾小管上皮细胞转分化的主要信号通路之一。

关 键 词:肾间质纤维化  肾小管上皮细胞  转分化  白细胞介素-18  p38MAPK

Interleukin-18-induced transdifferentiation in renal proximal tubular cells is mediated by activation of p38MAPK pathway
ZHANG Jun-feng,YAO Cui-wei,LIU Hua-feng,LIANG Dong,CHEN Xiao-wen. Interleukin-18-induced transdifferentiation in renal proximal tubular cells is mediated by activation of p38MAPK pathway[J]. Chinese journal of applied physiology, 2010, 0(2): 199-201
Authors:ZHANG Jun-feng  YAO Cui-wei  LIU Hua-feng  LIANG Dong  CHEN Xiao-wen
Affiliation:(Institute of Nephrology,Affiliated Hospital of Guangdong Medical College,Zhanjiang 524001,China)
Abstract:Objective:To explore the effect of p38MAPK signaling pathway in interleukin-18-induced transdifferentiation in renal proximal tubular cells.Methods:Human proximal tubular epithelial cell line (HK-2 cells) was cultured in vitro.After preincubated with SB203580(0,5,10,20 μmol/L) for 30 minutes,cells were exposed to IL-18(100 ng/ml) for 24,48 and 72 hours respectively.The expressions of α-smooth actin(α-SMA) in cultured HK-2 cells were assessed by RT-PCR and ELISA.Results:IL-18-induced expressions of α-SMA mRNA and protein were inhibited obviously by a dose-dependent manner when HK-2 cells were incubated with SB203580(0,5,10,20 μmol/L) and IL-18(100 ng/ml) for different time(P0.05).Conclusion:IL-18-induced transdifferentiation of renal tubular epithelial cells(RTECs) is suppressed obviously by blocking p38MAPK signaling pathways.IL-18-induced transdifferentiation of RTECs is probably mediated,at least in part,through the activation of p38MAPK signaling pathways.
Keywords:renal interstitial fibrosis  renal tubular epithelial cells  transdifferentiation  interleukin-18  p38MAPK
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