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Kwon, Hyug Moo
Immunometabolism and Cancer Lab
Research Interests
  • TonEBP, Obesity, Cancer, Chronic inflammatory diseases, Brain disorder, Kidney disorder, Genomic instability


Multiple cell death pathways are independently activated by lethal hypertonicity in renal epithelial cells

DC Field Value Language Choi, Soo Youn ko Lee-Kwon, Whaseon ko Lee, Hwan Hee ko Lee, Jun Ho ko Sanada, Satoru ko Kwon, H. Moo ko 2014-04-10T02:36:49Z - 2013-11-28 ko 2013-11 ko
dc.identifier.citation AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, v.305, no.10, pp.C1011 - C1020 ko
dc.identifier.issn 0363-6143 ko
dc.identifier.uri -
dc.description.abstract When hypertonicity is imposed with sufficient intensity and acuteness, cells die. Here we investigated the cellular pathways involved in death using a cell line derived from renal epithelium. We found that hypertonicity rapidly induced activation of an intrinsic cell death pathway- release of cytochrome c and activation of caspase-3 and caspase-9-and an extrinsic pathway-activation of caspase-8. Likewise, a lysosomal pathway of cell death characterized by partial lysosomal rupture and release of cathepsin B from lysosomes to the cytosol was also activated. Relationships among the pathways were examined using specific inhibitors. Caspase inhibitors did not affect cathepsin B release into the cytosol by hypertonicity. In addition, cathepsin B inhibitors and caspase inhibitors did not affect hyper-tonicity-induced cytochrome c release, suggesting that the three pathways were independently activated. Combined inhibition of caspases and cathepsin B conferred significantly more protection from hypertonicity-induced cell death than inhibition of caspase or cathepsin B alone, indicating that all the three pathways contributed to the hypertonicity-induced cell death. Similar pattern of sensitivity to the inhibitors was observed in two other cell lines derived from renal epithelia. We conclude that multiple cell death pathways are independently activated early in response to lethal hypertonic stress in renal epithelial cells. ko
dc.description.statementofresponsibility close -
dc.language 영어 ko
dc.title Multiple cell death pathways are independently activated by lethal hypertonicity in renal epithelial cells ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-84887588355 ko
dc.identifier.wosid 000327391700003 ko
dc.type.rims ART ko
dc.description.wostc 1 *
dc.description.scopustc 2 * 2014-10-18 * 2014-07-12 *
dc.identifier.doi 10.1152/ajpcell.00384.2012 ko
dc.identifier.url ko
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