EGFR-dependent ERK activation triggers hydrogen peroxide-induced apoptosis in OK renal epithelial cells
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- 作者：Ju Suk Lee (1)
Su Yung Kim (1) (3)
Chae Hwa Kwon (2)
Yong Keun Kim (2) (3) - 关键词：Hydrogen peroxide ; ERK activation ; Apoptosis ; Mitochondrial hyperpolarization ; Epidermal growth factor receptor ; Caspase activation ; Opossum kidney cells
- 刊名：Archives of Toxicology
- 出版年：2006
- 出版时间：June 2006
- 年：2006
- 卷：80
- 期：6
- 页码：337-346
- 全文大小：512KB
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Su Yung Kim (1) (3)
Chae Hwa Kwon (2)
Yong Keun Kim (2) (3)
1. Department of Pediatrics, College of Medicine, Pusan National University, 602-739, Pusan, South Korea
3. Medical Research Institute, College of Medicine, Pusan National University, 602-739, Pusan, South Korea
2. Department of Physiology, College of Medicine, Pusan National University, 602-739, Pusan, South Korea - ISSN：1432-0738
文摘
Oxidative stress induces activation of extracellular signal-regulated kinase (ERK), a member of the mitogen-activated protein kinase families. However, it is unclear in renal epithelial cells whether the ERK activation is involved in cell survival or cell death in H2O2-treated cells. The present study was undertaken to determine the role of the ERK activation in H2O2-induced apoptosis of renal epithelial cells using opossum kidney (OK) cells, an established proximal tubular epithelial cell line. H2O2 resulted in a time- and dose-dependent apoptosis of OK cells. H2O2 treatment caused marked sustained activation of ERK. The ERK activation was prevented by PD98059 and U0126, inhibitors of ERK1/2 upstream kinase MEK1/2. Apoptosis caused by H2O2 was prevented by U0126. Transient transfection with constitutive active MEK1 increased the H2O2-induced apoptosis, whereas transfection with dominant-negative mutants of MEK1 decreased the apoptosis. H2O2 produced hyperpolarization of mitochondrial membrane potential and activation of caspases-3. H2O2-induced ERK activation was inhibited by the Src family selective inhibitor PP2 and the epidermal growth factor receptor inhibitor AG1478. The presence of AG1478, but not PP2, prevented H2O2-induced cell death. Taken together, our findings suggest that the ERK activation mediated by epidermal growth factor receptor plays an active role in inducing H2O2-induced apoptosis of OK cells and functions upstream of mitochondria-dependent pathway to initiate the apoptotic signal.