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Expression of N iban in renal interstitial fibrosis
Author(s) -
Liu Jishi,
Qin Jiao,
Mei Wenjuan,
Zhang Hao,
Yuan Qiongjing,
Peng Zhangzhe,
Luo Renna,
Yuan Xiangning,
Huang Ling,
Tao Lijian
Publication year - 2014
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/nep.12266
Subject(s) - apoptosis , flow cytometry , tunel assay , western blot , renal cortex , transfection , immunohistochemistry , medicine , fibrosis , transforming growth factor , nephropathy , pathology , cancer research , kidney , biology , endocrinology , cell culture , immunology , gene , biochemistry , genetics , diabetes mellitus
Aim Apoptosis is one of the most important mechanisms underlying renal interstitial fibrosis. We identified the role of protein N iban in apoptosis of tumour cells. The purpose of this study was to assess the expression of N iban in renal interstitial fibrosis of humans and rats. Methods Immunohistochemistry was used to detect N iban in patients with obstructive nephropathy. Proteomics and gene array analysis were performed to screen different molecules involved in the pathophysiology of unilateral‐ureteral obstruction rats. We confirmed N iban using immunohistochemistry and W estern blot in renal cortex of UUO rats and HK ‐2 cells. TUNEL assay and flow cytometry revealed apoptosis of renal tubular cells. siRNA and overexpression plasmid were transfected specifically to study the possible function of N iban. Results N iban was decreased apparently in renal tubular cells of patients with obstructive nephropathy, compared with controls. N iban decreased in renal cortex of UUO rats and transforming growth factor‐β1 ( TGF ‐β1)‐stimulated HK ‐2 cells. siRNA of N iban increased apoptosis of HK ‐2 cells. TGF ‐β1 also increased apoptosis of HK ‐2 cells. Overexpression of N iban failed to diminish apoptosis of HK ‐2 cells induced by TGF ‐β1. Conclusions Niban decreased in renal tubular cells of patients of obstructive nephropathy, UUO rats and TGF ‐β1 stimulated HK ‐2 cells. Suppressing N iban increases apoptosis in HK ‐2 cells. N iban may be associated with apoptosis of HK ‐2 cells.