JNK-c-Jun signal pathway induces tubular epithelial-myofibroblast transition via downregulation of connexin 43 expression
10.3760/cma.j.issn.1001-7097.2011.12.013
- VernacularTitle:JNK-c-Jun信号通路下调连接蛋白43的表达引起肾小管上皮细胞转分化
- Author:
Xiaoxia HUANG
;
Changbin KE
;
Shoujun BAI
- Publication Type:Journal Article
- Keywords:
JNK mitogen-activated protein kinase;
Connexin 43;
Cell line transformed;
Renal tubular epithelial cells
- From:
Chinese Journal of Nephrology
2011;27(12):928-932
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the effect of JNK-c-Jun signal pathwayon connexin 43 (Cx43) expression and its role in renal tubular epithelial-myofibroblast transition (TEMT) induced by TGF-β1.Methods Normal rat kidney tubular epithelial cells(NRK-52E) were cultured in Dulbecco's modified eagle medium(DMEM) with 10％ fetal bovine serum,then were randomly divided into 3 groups: control group,TGF-β1 group (treated with TGF-β1 10 μg/L),and TGF-β1+SP600125 (selective JNK inhibitor,50 μmol/L) group. The protein expressions of JNK,c-Jun,α-SMA,Cx43 and E-cadherin were assayed by immunocytochemistry and Western blotting.The Cx43mRNA was assayed by RT-PCR.Gap junction intercellular communication(CJIC) was measured by fluorescence recovery after photobleaching assay(FRAP).Results TGF-β1increased the expressions of JNK,c-Jun and α-SMA(P＜0.05),reduced the expressions of Cx43 and E-cadherin (P＜0.05),and inhibited GJIC of NRK-52E(P ＜0.05).SP600125 could alleviate the above expressions changes and enhanced GJIC induced by TGF-β1.Conclusion JNK-c-Jun signal pathway induces TEMT ofNRK-52E treated with TGF-β1 viadown-regulation of connexin 43expression and inhibition of GJIC.
