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- W2095392012 abstract "We have shown previously that intracellular Ca+2chelation and calpain inhibitors block the influx of extracellular Ca+2and Cl−during the late phase of cell injury in renal proximal tubules (RPT) exposed to the mitochondrial inhibitor antimycin A. Since the endoplasmic reticulum (ER) is the major intracellular Ca+2storage site, ER Ca+2release/depletion may mediate the Ca+2influx and cell death. Treatment of RPT suspensions with thapsigargin, an ER Ca+2-ATPase inhibitor, increased cytosolic free Ca+2(Ca+2f) levels from 122 ± 7 to 322 ± 55 nM within 10 sec of addition followed by a return to control levels within 3 min. A 5-min pretreatment of RPT suspensions with thapsigargin blocked antimycin A- and hypoxia-induced influx of extracellular Ca+2and Cl−and the resulting cell death/lysis. These data suggest that ER Ca+2release/depletion during cell injury may trigger a signaling cascade that causes extracellular Ca+2influx followed by Cl−influx, cell swelling, and ultimately cell death/lysis." @default.
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- W2095392012 date "1997-11-01" @default.
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- W2095392012 title "Depletion of Endoplasmic Reticulum Calcium Stores Protects against Hypoxia- and Mitochondrial Inhibitor-Induced Cellular Injury and Death" @default.
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- W2095392012 doi "https://doi.org/10.1006/bbrc.1997.7606" @default.
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