Cellular & Molecular Biology Letters | |
Response gene to complement 32 regulates the G2/M phase checkpoint during renal tubular epithelial cell repair | |
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
【 预 览 】
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