There are no files associated with this item.
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.citation.endPage | C1020 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | C1011 | - |
dc.citation.title | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | - |
dc.citation.volume | 305 | - |
dc.contributor.author | Choi, Soo Youn | - |
dc.contributor.author | Lee-Kwon, Whaseon | - |
dc.contributor.author | Lee, Hwan Hee | - |
dc.contributor.author | Lee, Jun Ho | - |
dc.contributor.author | Sanada, Satoru | - |
dc.contributor.author | Kwon, H. Moo | - |
dc.date.accessioned | 2023-12-22T03:14:49Z | - |
dc.date.available | 2023-12-22T03:14:49Z | - |
dc.date.created | 2013-11-28 | - |
dc.date.issued | 2013-11 | - |
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. | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, v.305, no.10, pp.C1011 - C1020 | - |
dc.identifier.doi | 10.1152/ajpcell.00384.2012 | - |
dc.identifier.issn | 0363-6143 | - |
dc.identifier.scopusid | 2-s2.0-84887588355 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/4120 | - |
dc.identifier.url | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84887588355 | - |
dc.identifier.wosid | 000327391700003 | - |
dc.language | 영어 | - |
dc.publisher | AMER PHYSIOLOGICAL SOC | - |
dc.title | Multiple cell death pathways are independently activated by lethal hypertonicity in renal epithelial cells | - |
dc.type | Article | - |
dc.relation.journalWebOfScienceCategory | Cell Biology; Physiology | - |
dc.relation.journalResearchArea | Cell Biology; Physiology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.
Tel : 052-217-1404 / Email : scholarworks@unist.ac.kr
Copyright (c) 2023 by UNIST LIBRARY. All rights reserved.
ScholarWorks@UNIST was established as an OAK Project for the National Library of Korea.