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Abstract
BackgroundThe 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.MethodsNRK-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.ResultsThe 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.ConclusionsThe 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.
Highlights
The aim of this study was to evaluate the influence of response gene to complement 32 (RGC-32) on cell cycle progression in renal tubular epithelial cell injury
RGC-32 expression in the injured NRK-52E cells induced by Tumor necrosis factor-alpha (TNF-α) To determine whether TNF-α could cause acute cell injury, NRK-52E cells were cultured with TNF-α (10 ng/ml), and the expression level of neutrophil gelatinase-associated lipocalin (NGAL) was determined via western blotting and immunofluorescent staining (Fig. 1)
Immunofluorescent staining showed that increased NGAL levels in NRK52E cells treated with TNF-α for 24 h (Fig. 1c)
Summary
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. Available data suggest that acute and chronic kidney injury have become global health problems [1, 2]. The kidney has intrinsic repair capability through its surviving tubular epithelial cells [3]. Renal tubular epithelial tissue plays a vital role in the processes of post-injury germination and development, and in the prognosis of kidney injury [4,5,6]. The mechanisms of renal tubular injury and repair are known to be rather complex processes, involving cell cycle regulation, the signal transduction pathway and cell behavior changes. There is a lack of detailed studies on these mechanisms.
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