Yun-Lin Shen, Hua-Jie Liu, Lei Sun, Xiao-Ling Niu, Xin-Yu Kuang, Ping Wang, Sheng Hao, Wen-Yan Huang
Cellular & molecular biology letters 2016The 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.
Yun-Lin Shen, Hua-Jie Liu, Lei Sun, Xiao-Ling Niu, Xin-Yu Kuang, Ping Wang, Sheng Hao, Wen-Yan Huang. Response gene to complement 32 regulates the G2/M phase checkpoint during renal tubular epithelial cell repair. Cellular & molecular biology letters. 2016;21:19
PMID: 28536621
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