Journal
NEPHRON EXPERIMENTAL NEPHROLOGY
Volume 117, Issue 3, Pages E53-E61Publisher
KARGER
DOI: 10.1159/000320594
Keywords
Apoptosis; Human renal proximal tubule cells; Oxidative stress; PI3K/Akt signal transduction; Prostate apoptosis response factor-4; siRNA experiments
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Funding
- Natural Science Foundation of Jiangsu Province of China [BK2007244]
- National Natural Science Foundation of China [30872804]
- Medical Academic Key Talent Program of Jiangsu Province in China [RC2007050]
- Health Department of Jiangsu Province in China [H200901]
- China Postdoctoral Science Foundation [20070411062]
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Background: Oxidative stress is an important inducer of cell apoptosis and plays a key role in the development of renal inflammation. The prostate apoptosis response factor-4 (Par-4) gene was originally identified in prostate cells undergoing apoptosis. Subsequently, Par-4 was found to possess potent pro-apoptotic activity in various cellular systems. However, it remains unclear whether Par-4 is involved in oxidant injury of renal tubular epithelial cells. Aims: To determine the role of Par-4 in renal proximal tubular cell apoptosis induced by oxidative stress. Methods: Par-4 gene expression was silenced by small interfering RNA. Renal proximal tubular cells were then exposed to hydrogen peroxide and the effect of Par-4 silencing on apoptosis and expression of phosphorylated Akt and vascular endothelial growth factor was determined. Results: Hydrogen peroxide induced apoptosis and increased Par-4 expression in human renal proximal tubular epithelial cells. Par-4 silencing significantly protected renal proximal tubular cells from apoptosis via activating the PI3K/Akt signaling pathway as Akt phosphorylation was enhanced. Par-4 silencing also ameliorated the downregulation of vascular endothelial growth factor expression induced by oxidative stress. Conclusion: Par-4 gene silencing resulted in PI3K/Akt signaling-dependent inhibition of renal proximal tubular cell apoptosis following oxidative stress. Copyright (C) 2010 S. Karger AG, Basel
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