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• W2073174042 abstract "Abstract Sub‐lethal activation of cell death processes initiate pro‐survival signaling cascades. As intracellular Zn 2+ liberation mediates neuronal death pathways, we tested whether a sub‐lethal increase in free Zn 2+ could also trigger neuroprotection. Neuronal free Zn 2+ transiently increased following preconditioning, and was both necessary and sufficient for conferring excitotoxic tolerance. Lethal exposure to NMDA led to a delayed increase in Zn 2+ that contributed significantly to excitotoxicity in non‐preconditioned neurons, but not in tolerant neurons, unless preconditioning‐induced free Zn 2+ was chelated. Thus, preconditioning may trigger the expression of Zn 2+ ‐regulating processes, which, in turn, prevent subsequent Zn 2+ ‐mediated toxicity. Indeed, preconditioning increased Zn 2+ ‐regulated gene expression in neurons. Examination of the molecular signaling mechanism leading to this early Zn 2+ signal revealed a critical role for protein kinase C (PKC) activity, suggesting that PKC may act directly on the intracellular source of Zn 2+ . We identified a conserved PKC phosphorylation site at serine‐32 (S32) of metallothionein (MT) that was important in modulating Zn 2+ ‐regulated gene expression and conferring excitotoxic tolerance. Importantly, we observed increased PKC‐induced serine phosphorylation in immunopurified MT1, but not in mutant MT1(S32A). These results indicate that neuronal Zn 2+ serves as an important, highly regulated signaling component responsible for the initiation of a neuroprotective pathway." @default.
• W2073174042 created "2016-06-24" @default.
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• W2073174042 date "2009-06-15" @default.
• W2073174042 modified "2023-10-16" @default.
• W2073174042 title "Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning" @default.
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• W2073174042 doi "https://doi.org/10.1111/j.1471-4159.2009.06106.x" @default.
• W2073174042 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2719843" @default.
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