Role of Bcl-xL induction in HGF-mediated renal epithelial cell survival after oxidant stress.

摘要: Hepatocyte growth factor (HGF) is known to promote renal epithelial cell survival by dual mechanisms involving Bad phosphorylation and Bcl-xL induction. However, it remains elusive as the relative contributions of these two events HGF-mediated cytoprotection. Here we investigated role mechanism HGF in protecting cells from death induced oxidant stress both vitro vivo. Simultaneous incubation human kidney proximal tubular (HKC-8) with failed protect them stress-induced death, even though was capable inducing endogenous Akt phosphorylation. pre-incubation HKC-8 for 48 hours dramatically promoted their prevented caspase-3 cleavage activation H(2)O(2). A close association between induction effective cytoprotection observed after H(2)O(2) treatment. Furthermore, ectopic expression exogenous via adenoviral vector H(2)O(2)-triggered activation. In a mouse model acute injury ischemia/reperfusion, pre-administration drastically apoptosis largely preserved function, whereas much less protective effect when gene given immediately ischemic injury. These results suggest that plays an imperative mediating challenge.