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Preparation and evaluation of anti‐renal fibrosis activity of novel truncated TGF‐β receptor type II
Author(s) -
Liu Haifeng,
Zhang Zhongmin,
Li Yuting,
Wang Xiaoli,
Zhang Yufei,
Chu Yanhui,
Yuan Xiaohuan,
Wang Xiaohua
Publication year - 2018
Publication title -
biotechnology and applied biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.468
H-Index - 70
eISSN - 1470-8744
pISSN - 0885-4513
DOI - 10.1002/bab.1667
Subject(s) - transforming growth factor , fibrosis , receptor , kidney , chemistry , medicine
Abstract Production of excessive transforming growth factor‐beta 1 (TGF‐β1) with elevated TGF‐β1 activity has been implicated in renal fibrosis via renal epithelial cells activation and collagen deposition. As such, attenuating the binding of TGF‐β1 to its receptor TGF‐beta receptor type II (TGF‐βRII) in TGF‐β1‐dependent signaling is an attractive target for the control of renal fibrosis. Here, we verified the interaction between novel truncated human TGF‐βRII (thTβRII, Thr23‐Gln166) and TGF‐β1, prepared thTβRII in Escherichia coli , and assessed the effects of thTβRII on TGF‐β1‐induced human kidney epithelial cells (HK‐2) and unilateral ureteral obstruction (UUO) model of renal fibrosis. Our data showed that thTβRII accounted for up to 20% of the total protein and 40% of the inclusion bodies of whole cell lysates under the optimal conditions (0.8 mM IPTG and 25°C for 6 H). Most of the expressed protein in inclusion body was refolded by dialysis refolding procedures and purified by Ni 2+ ‐IDA affinity chromatography. Furthermore, thTβRII decreased type I collagen and α‐smooth muscle actin protein expression in TGF‐β1‐induced HK‐2 cells, and ameliorated kidney morphology and fibrotic responses in fibrosis animal. These findings indicate that thTβRII holds great promise for developing new treatments for renal fibrosis.