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10.1016/j.neulet.2019.134315 http://scihub22266oqcxt.onion/10.1016/j.neulet.2019.134315 31185281!ä!31185281 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31185281&cmd=llinks): Failed to open stream: HTTP request failed! 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Intracellular labile zinc is a determinant of vulnerability of cultured astrocytes to oxidative stress |pdf=|usr=}}{{31185281}} gab.com Text Intracellular labile zinc is a determinant of vulnerability of cultured astrocytes to oxidative stress JO: Neurosci Lett http://www.kidney.de/pget.php?&tw=1&pmid=31185281 #FOAvip Recently, we found that treatment of cultured mouse astrocytes of ddY-strain mice (ddY-astrocytes) with 400?muM H(2)O(2) for 24?h increased the intracellular labile zinc level without cell toxicity. In contrast, 170?muM H(2)O(2) for 12?h is reported to kill mouse astrocytes obtained from C57BL/6-strain mice (C57BL/6-astrocytes) with an increase in intracellular labile zinc. To clarify this discrepancy, we compared the intracellular zinc levels and cell toxicity in H(2)O(2)-treated ddY- and C57BL/6-astrocytes. Exposure of C57BL/6-astrocytes to 170 or 400?muM H(2)O(2) for 12?h dose-dependently decreased the cell viability and administration of plasma membrane-permeable zinc chelator TPEN prevented the 170?muM H(2)O(2)-induced astrocyte death, while neither concentration of H(2)O(2) killed ddY-astrocytes. The intracellular zinc level in H(2)O(2)-treated C57BL/6-astrocytes was higher than that in H(2)O(2)-treated ddY-astrocytes, and this increase was suppressed by TPEN. There was no apparent difference in the expression levels of zinc transporters ZIPs and ZnTs between the two types of astrocytes, while expression of zinc releasable channel TRPM7 was found on the plasma membrane in ddY-astrocytes, but not in C57BL/6-astrocytes, although the total cellular expression levels were almost the same. In addition, a TRPM7 blocker, 2-aminoethoxydiphenyl borate, increased the intracellular zinc level in H(2)O(2)-treated ddY-, but not C57BL/6-astrocytes. Collectively, it is suggested that vulnerability of astrocytes to oxidative stress depends on an increased level of intracellular labile zinc, and TRPM7 localized on the plasma membrane contributes, at least in part, to ameliorate the cell injury by decreasing the zinc level. Twit Text FOAVip Intracellular labile zinc is a determinant of vulnerability of cultured astrocytes to oxidative stress ????Neurosci Lett http://www.kidney.de/pget.php?&tw=1&pmid=31185281 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31185281 #FOAvip English Wikipedia <ref>{{Cite pmid|31185281}}</ref> Intracellular labile zinc is a determinant of vulnerability of cultured astrocytes to oxidative stress #MMPMID31185281 Furuta T; Ohishi A; Nagasawa K Neurosci Lett 2019[Aug]; 707 (ä): 134315 PMID31185281show ga Recently, we found that treatment of cultured mouse astrocytes of ddY-strain mice (ddY-astrocytes) with 400?muM H(2)O(2) for 24?h increased the intracellular labile zinc level without cell toxicity. In contrast, 170?muM H(2)O(2) for 12?h is reported to kill mouse astrocytes obtained from C57BL/6-strain mice (C57BL/6-astrocytes) with an increase in intracellular labile zinc. To clarify this discrepancy, we compared the intracellular zinc levels and cell toxicity in H(2)O(2)-treated ddY- and C57BL/6-astrocytes. Exposure of C57BL/6-astrocytes to 170 or 400?muM H(2)O(2) for 12?h dose-dependently decreased the cell viability and administration of plasma membrane-permeable zinc chelator TPEN prevented the 170?muM H(2)O(2)-induced astrocyte death, while neither concentration of H(2)O(2) killed ddY-astrocytes. The intracellular zinc level in H(2)O(2)-treated C57BL/6-astrocytes was higher than that in H(2)O(2)-treated ddY-astrocytes, and this increase was suppressed by TPEN. There was no apparent difference in the expression levels of zinc transporters ZIPs and ZnTs between the two types of astrocytes, while expression of zinc releasable channel TRPM7 was found on the plasma membrane in ddY-astrocytes, but not in C57BL/6-astrocytes, although the total cellular expression levels were almost the same. In addition, a TRPM7 blocker, 2-aminoethoxydiphenyl borate, increased the intracellular zinc level in H(2)O(2)-treated ddY-, but not C57BL/6-astrocytes. Collectively, it is suggested that vulnerability of astrocytes to oxidative stress depends on an increased level of intracellular labile zinc, and TRPM7 localized on the plasma membrane contributes, at least in part, to ameliorate the cell injury by decreasing the zinc level. |*Oxidative Stress[MESH] |Animals[MESH] |Astrocytes/drug effects/*metabolism[MESH] |Cell Death[MESH] |Cell Survival[MESH] |Cells, Cultured[MESH] |Cerebral Cortex/cytology[MESH] |Chlorides/pharmacology[MESH] |Hydrogen Peroxide/pharmacology[MESH] |Intracellular Space/metabolism[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Species Specificity[MESH] |TRPM Cation Channels/metabolism[MESH] |Zinc Compounds/pharmacology[MESH]Intracellular labile zinc is a determinant of vulnerability of culture(epmc).pdf DeepDyve Pubget Overpricing