Abstract
Oxidative stress plays an important role in the induction of mesangial cell (MC) injury. In the present study, we evaluated the molecular mechanism involved in hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced MC apoptosis. In addition, we examined the role of heme oxygenase-1 (HO-1) in hepatocyte growth factor (HGF)-modulated, H<sub>2</sub>O<sub>2</sub>-induced MC injury. H<sub>2</sub>O<sub>2</sub> promoted (p < 0.001) mouse MC (MMC) apoptosis. This effect of H<sub>2</sub>O<sub>2</sub> was associated with translocation of cytochrome c from the mitochondrial to the cytosolic compartment. In addition, a caspase-9 inhibitor partially attenuated this effect of H<sub>2</sub>O<sub>2</sub>. These findings suggest that H<sub>2</sub>O<sub>2</sub>-induced MMC apoptosis is mediated through the mitochondrial pathway. HGF not only prevented H<sub>2</sub>O<sub>2</sub>-induced MMC apoptosis, but also inhibited H<sub>2</sub>O<sub>2</sub>-induced translocation of cytochrome c from the mitochondrial to the cytosolic compartment. HGF also promoted the expression of HO-1 by MMCs; interestingly, hemin inhibited (p < 0.001) H<sub>2</sub>O<sub>2</sub>-induced MMC apoptosis. On the other hand, zinc protoporphyrin inhibited the protective influence of HGF on H<sub>2</sub>O<sub>2</sub>-induced MMC apoptosis. These findings suggest that H<sub>2</sub>O<sub>2</sub>-induced apoptosis occurs through the mitochondrial pathway. HGF provides protection against H<sub>2</sub>O<sub>2</sub>-induced MMC apoptosis through induction of HO-1.
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