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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

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

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dc.contributor.author Choi, Soo Youn ko
dc.contributor.author Lee-Kwon, Whaseon ko
dc.contributor.author Lee, Hwan Hee ko
dc.contributor.author Lee, Jun Ho ko
dc.contributor.author Sanada, Satoru ko
dc.contributor.author Kwon, H. Moo ko
dc.date.available 2014-04-10T02:36:49Z -
dc.date.created 2013-11-28 ko
dc.date.issued 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 https://scholarworks.unist.ac.kr/handle/201301/4120 -
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.publisher AMER PHYSIOLOGICAL SOC 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 *
dc.date.tcdate 2014-10-18 *
dc.date.scptcdate 2014-07-12 *
dc.identifier.doi 10.1152/ajpcell.00384.2012 ko
dc.identifier.url http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84887588355 ko
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