K-ATP channel block prevents proteasome inhibitor-induced apoptosis in differentiated PC12 cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Nam, Yoon Jeong | - |
dc.contributor.author | Lee, Da Hee | - |
dc.contributor.author | Lee, Min Sung | - |
dc.contributor.author | Lee, Chung Soo | - |
dc.date.accessioned | 2023-03-08T18:30:15Z | - |
dc.date.available | 2023-03-08T18:30:15Z | - |
dc.date.issued | 2015-10 | - |
dc.identifier.issn | 0014-2999 | - |
dc.identifier.issn | 1879-0712 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/64467 | - |
dc.description.abstract | Dysfunction of the proteasome system has been suggested to be implicated in neuronal degeneration. Modulation of K-ATP channels appears to affect the viability of neuronal cells exposed to toxic insults. However, the effect of K-ATP channel blockers on the neuronal cell death mediated by proteasome inhibition has not been studied. The present study investigated the effect of K-ATP channel blockers on proteasome inhibitor-induced apoptosis in differentiated PC12 cells and SH-SY5Y cells. 5-Hydroxydecanoate (a selective K-ATP channel blocker) and glibenclamide (a cell surface and mitochondrial K-ATP channel inhibitor) reduced the proteasome inhibitor-induced apoptosis. Addition of the K-ATP channel blockers attenuated the proteasome inhibitor-induced changes in the levels of apoptosis-related proteins, the loss of the mitochondrial transmembrane potential, the increase in the formation of reactive oxygen species and the depletion of glutathione in both cell lines. The results show that K-ATP channel blockers may attenuate proteasome inhibitor-induced apoptosis in PC12 cells by suppressing activation of the mitochondrial pathway and of the caspase-8- and Bid-dependent pathways. The preventive effect appears to be associated with the inhibition of the formation of reactive oxygen species and the depletion of glutathione. K-ATP channel blockade appears to prevent proteasome inhibition-induced neuronal cell death. (C) 2015 Elsevier B.V. All rights reserved. | - |
dc.format.extent | 10 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | ELSEVIER SCIENCE BV | - |
dc.title | K-ATP channel block prevents proteasome inhibitor-induced apoptosis in differentiated PC12 cells | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.ejphar.2015.06.049 | - |
dc.identifier.bibliographicCitation | EUROPEAN JOURNAL OF PHARMACOLOGY, v.764, pp 582 - 591 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000362987800070 | - |
dc.identifier.scopusid | 2-s2.0-84938614612 | - |
dc.citation.endPage | 591 | - |
dc.citation.startPage | 582 | - |
dc.citation.title | EUROPEAN JOURNAL OF PHARMACOLOGY | - |
dc.citation.volume | 764 | - |
dc.type.docType | Article | - |
dc.publisher.location | 네델란드 | - |
dc.subject.keywordAuthor | Proteasome inhibitors | - |
dc.subject.keywordAuthor | K-ATP channel blockers | - |
dc.subject.keywordAuthor | PC12 cells | - |
dc.subject.keywordAuthor | Apoptosis-relatecl proteins | - |
dc.subject.keywordAuthor | Protection | - |
dc.subject.keywordPlus | SENSITIVE POTASSIUM CHANNELS | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | MITOCHONDRIAL DYSFUNCTION | - |
dc.subject.keywordPlus | PERMEABILITY TRANSITION | - |
dc.subject.keywordPlus | MOLECULAR CHAPERONES | - |
dc.subject.keywordPlus | THERAPEUTIC TARGETS | - |
dc.subject.keywordPlus | CANCER CELLS | - |
dc.subject.keywordPlus | NEURONS | - |
dc.subject.keywordPlus | DIAZOXIDE | - |
dc.subject.keywordPlus | GROWTH | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.