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Effect of pro-inflammatory interleukin-17A on epithelial cell phenotype inversion in HK-2 cells in vitro Volume 27, numéro 2, June 2016

Illustrations


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Auteurs
1 Department of Nephrology, Affiliated Hospital of Luzhou Medical College, Luzhou City 646000,Sichuan Province, China
2 Department of Nephrology, West China Hospital of Sichuan University, Chengdu City610041, Sichuan Province, China
3 Department of Nephrology, Shanghai general hospital, Shanghai Jiao Tong University, Shanghai City 200080, China
4 Department of Central Service, West China Hospital of Sichuan University, Chengdu City 610041, Sichuan Province, China
5 State Key Laboratory of Biotherapy of Human Disease, West China Hospital, Sichuan University, Chengdu City 610041, Sichuan Province, China.
6 People's Hospital of Jianyang, Ziyang City 641400, Sichuan Province, China.
* Correspondence
a The authors contributed equally to this article.

Background

Renal interstitial fibrosis (RIF) is a pathological change common to a variety of chronic renal diseases, ultimately progressing to end-stage renal failure. It is believed that epithelial cell phenotype inversion plays an important role in RIF, which is characterized by expression of the mesenchymal maker α-SMA, loss of the epithelial maker E-cadherin, and enhanced secretion of extracellular matrix. IL-17, a newly discovered pro-inflammatory cytokine, has recently been reported to play an important role in tissue fibrosis, involving pulmonary, liver, intestine and skin tissues. This study aimed to investigate whether IL-17A, a member of the IL-17 family, can induce epithelial cell phenotype inversion, and to explore the molecular mechanism of this phenotype inversion, in vitro.