Akt and Erk1/2 activate the ornithine decarboxylase/polyamine system in cardioprotective ischemic preconditioning in rats: the role of mitochondrial permeability transition pores.
作者： Hao Zhang , Guo Xue , Weihua Zhang , Lina Wang , Hong Li
DOI: 10.1007/S11010-014-1964-Z
关键词:
摘要: Ornithine decarboxylase (ODC) is the first rate-limiting enzyme in polyamine biosynthesis, which essential for cell survival. We hypothesized that ODC/polyamine system involved ischemic preconditioning (IPC)-mediated cardioprotection through activation of Erk1/2 and Akt inhibition mitochondrial permeability transition (mPT). Isolated rat hearts were subjected to 40 min ischemia either with or without IPC (3 cycles 5-min global ischemia), ODC protein expression, content, phosphorylation evaluated after 30 reperfusion. significantly upregulated pathway, promoted phosphorylation, reduced infarct size heart dysfunction An inhibitor ODC, α-difluoromethylornithine (DFMO), abolished IPC-induced cardioprotection. Moreover, using PD98059 wortmannin downregulated system. In separate studies, Ca2+ load required open mPT pore was lower DFMO-treated cardiac mitochondria than from hearts. Furthermore, spermine spermidine inhibited induced by CaCl2. These results suggest upregulates mediates cardioprotection, may depend on phosphorylation/activation during
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