Differential effect of calmodulin antagonists on MG132-induced mitochondrial dysfunction and cell death in PC12 cells
DC Field | Value | Language |
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dc.contributor.author | Lee, Chung Soo | - |
dc.contributor.author | Han, Eun Sook | - |
dc.contributor.author | Han, Young Su | - |
dc.contributor.author | Bang, Hyoweon | - |
dc.date.available | 2019-05-30T07:36:01Z | - |
dc.date.issued | 2005-10 | - |
dc.identifier.issn | 0361-9230 | - |
dc.identifier.issn | 1873-2747 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/24500 | - |
dc.description.abstract | Defects in proteasome function have been suggested to be involved in the pathogenesis of neurodegenerative diseases. We examined the effect of calmodulin antagonists on proteasome inhibitor-induced mitochondrial dysfunction and cell viability loss in undifferentiated PC12 cells. Caspase inhibitors (z-IETD.fmk, z-LEHD.fmk and z-DQMD.fmk) and antioxidants attenuated cell death and decrease in GSH contents in PC12 cells treated with 20 mu M MG132, a proteasome inhibitor. Calmodulin antagonists (trifluoperazine, W-7 and calmidazolium) had a differential inhibitory effect on the MG132-induced cell death and GSH depletion depending on concentration with a maximal inhibitory effect at 0.5-1 mu M. Addition of trifluoperazine and W-7 reduced the MG132-induced nuclear damage, loss of the mitochondrial transmembrane potential followed by cytochrome c release, formation of reactive oxygen species and elevation of intracellular Ca2+ levels in PC12 cells. Calmodulin antagonists at 5 mu M exhibited a cytotoxic effect on PC12 cells but attenuated the cytotoxicity of MG132. The results suggest that the toxicity of MG132 on PC12 cells is mediated by activation of caspase-8, -9 and -3. Trifluoperazine and W-7 at the concentrations of 0.5-1 mu M may attenuate the MG132-induced viability loss in PC12 cells by suppressing change in the mitochondrial membrane permeability and by lowering of the intracellular Ca2+ levels as well as calmodulin inhibition. (c) 2005 Elsevier Inc. All rights reserved. | - |
dc.format.extent | 10 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | - |
dc.title | Differential effect of calmodulin antagonists on MG132-induced mitochondrial dysfunction and cell death in PC12 cells | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.brainresbull.2005.07.003 | - |
dc.identifier.bibliographicCitation | BRAIN RESEARCH BULLETIN, v.67, no.3, pp 225 - 234 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000232172200009 | - |
dc.identifier.scopusid | 2-s2.0-24144467440 | - |
dc.citation.endPage | 234 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 225 | - |
dc.citation.title | BRAIN RESEARCH BULLETIN | - |
dc.citation.volume | 67 | - |
dc.type.docType | Article | - |
dc.publisher.location | 영국 | - |
dc.subject.keywordAuthor | calmodulin antagonists | - |
dc.subject.keywordAuthor | MG132 | - |
dc.subject.keywordAuthor | mitochondrial membrane permeability | - |
dc.subject.keywordAuthor | cell injury | - |
dc.subject.keywordAuthor | PC12 cells | - |
dc.subject.keywordPlus | OXYGEN SPECIES PRODUCTION | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | PROTEASOME INHIBITORS | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | PERMEABILITY TRANSITION | - |
dc.subject.keywordPlus | INDEPENDENT APOPTOSIS | - |
dc.subject.keywordPlus | GLIOMA-CELLS | - |
dc.subject.keywordPlus | CALCIUM | - |
dc.subject.keywordPlus | ASTROCYTES | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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