Response gene to complement 32 regulates the G2/M phase checkpoint during renal tubular epithelial cell repair

Cellular & Molecular Biology Letters

Sheng Hao¹  Xin-yu Kuang¹  Yun-lin Shen¹  Hua-jie Liu¹  Xiao-ling Niu¹  Lei Sun¹  Ping Wang¹  Wen-yan Huang¹ 

[1] Department of Nephrology and Rheumatology, Shanghai Children’s Hospital, Shanghai Jiao Tong University, Shanghai, China$$

关键词: Response gene to complement 32;    Cell cycle;    G2/M phase;    Tumor necrosis factor-alpha;    Tubulointerstitial fibrosis;    Tubular epithelial cell repair;   

DOI  :  10.1186/s11658-016-0021-1

学科分类：分子生物学，细胞生物学和基因

来源: Uniwersytet Wroclawski * Wydzial Biotechnologii / University of Wroclaw, Faculty of Biotechnology

【 摘 要 】

The aim of this study was to evaluate the influence of RGC-32 (response gene to complement 32) on cell cycle progression in renal tubular epithelial cell injury. NRK-52E cells with overexpressed or silenced RGC-32 were constructed via transient transfection with RGC-32 expression plasmid and RGC-32 siRNA plasmid, and the cell cycle distribution was determined. The expression levels of fibrosis factors, including smooth muscle action (α-SMA), fibronectin (FN) and E-cadherin, were assessed in cells with silenced RGC-32. The cells were injured via TNF-α treatment, and the injury was detectable by the enhanced expression of neutrophil gelatinase-associated lipocalin (NGAL). RGC-32 expression also increased significantly. The number of cells at G2/M phase increased dramatically in RGC-32 silenced cells, indicating that RGC-32 silencing induced G2/M arrest. In addition, after treatment with TNF-α, the NRK-52E cells with silenced RGC-32 showed significantly increased expression of α-SMA and FN, but decreased expression of E-cadherin. The results of this study suggest that RGC-32 probably has an important impact on the repair process of renal tubular epithelial cells in vitro by regulating the G2/M phase checkpoint, cell fibrosis and cell adhesion. However, the exact mechanism needs to be further elucidated.

【 授权许可】

Unknown