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Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning
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| Zeitschriftentitel: | Journal of Neurochemistry |
|---|---|
| Personen und Körperschaften: | , , , , |
| In: | Journal of Neurochemistry, 110, 2009, 1, S. 106-117 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Aras, Mandar A. Hara, Hirokazu Hartnett, Karen A. Kandler, Karl Aizenman, Elias Aras, Mandar A. Hara, Hirokazu Hartnett, Karen A. Kandler, Karl Aizenman, Elias |
|---|---|
| author |
Aras, Mandar A. Hara, Hirokazu Hartnett, Karen A. Kandler, Karl Aizenman, Elias |
| spellingShingle |
Aras, Mandar A. Hara, Hirokazu Hartnett, Karen A. Kandler, Karl Aizenman, Elias Journal of Neurochemistry Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning Cellular and Molecular Neuroscience Biochemistry |
| author_sort |
aras, mandar a. |
| spelling |
Aras, Mandar A. Hara, Hirokazu Hartnett, Karen A. Kandler, Karl Aizenman, Elias 0022-3042 1471-4159 Wiley Cellular and Molecular Neuroscience Biochemistry http://dx.doi.org/10.1111/j.1471-4159.2009.06106.x <jats:title>Abstract</jats:title><jats:p>Sub‐lethal activation of cell death processes initiate pro‐survival signaling cascades. As intracellular Zn<jats:sup>2+</jats:sup> liberation mediates neuronal death pathways, we tested whether a sub‐lethal increase in free Zn<jats:sup>2+</jats:sup> could also trigger neuroprotection. Neuronal free Zn<jats:sup>2+</jats:sup> 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<jats:sup>2+</jats:sup> that contributed significantly to excitotoxicity in non‐preconditioned neurons, but not in tolerant neurons, unless preconditioning‐induced free Zn<jats:sup>2+</jats:sup> was chelated. Thus, preconditioning may trigger the expression of Zn<jats:sup>2+</jats:sup>‐regulating processes, which, in turn, prevent subsequent Zn<jats:sup>2+</jats:sup>‐mediated toxicity. Indeed, preconditioning increased Zn<jats:sup>2+</jats:sup>‐regulated gene expression in neurons. Examination of the molecular signaling mechanism leading to this early Zn<jats:sup>2+</jats:sup> signal revealed a critical role for protein kinase C (PKC) activity, suggesting that PKC may act directly on the intracellular source of Zn<jats:sup>2+</jats:sup>. We identified a conserved PKC phosphorylation site at serine‐32 (S32) of metallothionein (MT) that was important in modulating Zn<jats:sup>2+</jats:sup>‐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<jats:sup>2+</jats:sup> serves as an important, highly regulated signaling component responsible for the initiation of a neuroprotective pathway.</jats:p> Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning Journal of Neurochemistry |
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| title |
Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_unstemmed |
Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_full |
Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_fullStr |
Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_full_unstemmed |
Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_short |
Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_sort |
protein kinase c regulation of neuronal zinc signaling mediates survival during preconditioning |
| topic |
Cellular and Molecular Neuroscience Biochemistry |
| url |
http://dx.doi.org/10.1111/j.1471-4159.2009.06106.x |
| publishDate |
2009 |
| physical |
106-117 |
| description |
<jats:title>Abstract</jats:title><jats:p>Sub‐lethal activation of cell death processes initiate pro‐survival signaling cascades. As intracellular Zn<jats:sup>2+</jats:sup> liberation mediates neuronal death pathways, we tested whether a sub‐lethal increase in free Zn<jats:sup>2+</jats:sup> could also trigger neuroprotection. Neuronal free Zn<jats:sup>2+</jats:sup> 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<jats:sup>2+</jats:sup> that contributed significantly to excitotoxicity in non‐preconditioned neurons, but not in tolerant neurons, unless preconditioning‐induced free Zn<jats:sup>2+</jats:sup> was chelated. Thus, preconditioning may trigger the expression of Zn<jats:sup>2+</jats:sup>‐regulating processes, which, in turn, prevent subsequent Zn<jats:sup>2+</jats:sup>‐mediated toxicity. Indeed, preconditioning increased Zn<jats:sup>2+</jats:sup>‐regulated gene expression in neurons. Examination of the molecular signaling mechanism leading to this early Zn<jats:sup>2+</jats:sup> signal revealed a critical role for protein kinase C (PKC) activity, suggesting that PKC may act directly on the intracellular source of Zn<jats:sup>2+</jats:sup>. We identified a conserved PKC phosphorylation site at serine‐32 (S32) of metallothionein (MT) that was important in modulating Zn<jats:sup>2+</jats:sup>‐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<jats:sup>2+</jats:sup> serves as an important, highly regulated signaling component responsible for the initiation of a neuroprotective pathway.</jats:p> |
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| author | Aras, Mandar A., Hara, Hirokazu, Hartnett, Karen A., Kandler, Karl, Aizenman, Elias |
| author_facet | Aras, Mandar A., Hara, Hirokazu, Hartnett, Karen A., Kandler, Karl, Aizenman, Elias, Aras, Mandar A., Hara, Hirokazu, Hartnett, Karen A., Kandler, Karl, Aizenman, Elias |
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| description | <jats:title>Abstract</jats:title><jats:p>Sub‐lethal activation of cell death processes initiate pro‐survival signaling cascades. As intracellular Zn<jats:sup>2+</jats:sup> liberation mediates neuronal death pathways, we tested whether a sub‐lethal increase in free Zn<jats:sup>2+</jats:sup> could also trigger neuroprotection. Neuronal free Zn<jats:sup>2+</jats:sup> 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<jats:sup>2+</jats:sup> that contributed significantly to excitotoxicity in non‐preconditioned neurons, but not in tolerant neurons, unless preconditioning‐induced free Zn<jats:sup>2+</jats:sup> was chelated. Thus, preconditioning may trigger the expression of Zn<jats:sup>2+</jats:sup>‐regulating processes, which, in turn, prevent subsequent Zn<jats:sup>2+</jats:sup>‐mediated toxicity. Indeed, preconditioning increased Zn<jats:sup>2+</jats:sup>‐regulated gene expression in neurons. Examination of the molecular signaling mechanism leading to this early Zn<jats:sup>2+</jats:sup> signal revealed a critical role for protein kinase C (PKC) activity, suggesting that PKC may act directly on the intracellular source of Zn<jats:sup>2+</jats:sup>. We identified a conserved PKC phosphorylation site at serine‐32 (S32) of metallothionein (MT) that was important in modulating Zn<jats:sup>2+</jats:sup>‐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<jats:sup>2+</jats:sup> serves as an important, highly regulated signaling component responsible for the initiation of a neuroprotective pathway.</jats:p> |
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| spelling | Aras, Mandar A. Hara, Hirokazu Hartnett, Karen A. Kandler, Karl Aizenman, Elias 0022-3042 1471-4159 Wiley Cellular and Molecular Neuroscience Biochemistry http://dx.doi.org/10.1111/j.1471-4159.2009.06106.x <jats:title>Abstract</jats:title><jats:p>Sub‐lethal activation of cell death processes initiate pro‐survival signaling cascades. As intracellular Zn<jats:sup>2+</jats:sup> liberation mediates neuronal death pathways, we tested whether a sub‐lethal increase in free Zn<jats:sup>2+</jats:sup> could also trigger neuroprotection. Neuronal free Zn<jats:sup>2+</jats:sup> 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<jats:sup>2+</jats:sup> that contributed significantly to excitotoxicity in non‐preconditioned neurons, but not in tolerant neurons, unless preconditioning‐induced free Zn<jats:sup>2+</jats:sup> was chelated. Thus, preconditioning may trigger the expression of Zn<jats:sup>2+</jats:sup>‐regulating processes, which, in turn, prevent subsequent Zn<jats:sup>2+</jats:sup>‐mediated toxicity. Indeed, preconditioning increased Zn<jats:sup>2+</jats:sup>‐regulated gene expression in neurons. Examination of the molecular signaling mechanism leading to this early Zn<jats:sup>2+</jats:sup> signal revealed a critical role for protein kinase C (PKC) activity, suggesting that PKC may act directly on the intracellular source of Zn<jats:sup>2+</jats:sup>. We identified a conserved PKC phosphorylation site at serine‐32 (S32) of metallothionein (MT) that was important in modulating Zn<jats:sup>2+</jats:sup>‐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<jats:sup>2+</jats:sup> serves as an important, highly regulated signaling component responsible for the initiation of a neuroprotective pathway.</jats:p> Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning Journal of Neurochemistry |
| spellingShingle | Aras, Mandar A., Hara, Hirokazu, Hartnett, Karen A., Kandler, Karl, Aizenman, Elias, Journal of Neurochemistry, Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning, Cellular and Molecular Neuroscience, Biochemistry |
| title | Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_full | Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_fullStr | Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_full_unstemmed | Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_short | Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_sort | protein kinase c regulation of neuronal zinc signaling mediates survival during preconditioning |
| title_unstemmed | Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning |
| topic | Cellular and Molecular Neuroscience, Biochemistry |
| url | http://dx.doi.org/10.1111/j.1471-4159.2009.06106.x |