Inhibition of MPP+-induced mitochondrial damage and cell death by trifluoperazine and W-7 in PC12 cells
DC Field | Value | Language |
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dc.contributor.author | Lee, Chung Soo | - |
dc.contributor.author | Park, Se Young | - |
dc.contributor.author | Ko, Hyun Hee | - |
dc.contributor.author | Song, Jin Ho | - |
dc.contributor.author | Shin, Yong Kyoo | - |
dc.contributor.author | Han, Eun Sook | - |
dc.date.available | 2019-05-30T08:33:06Z | - |
dc.date.issued | 2005-01 | - |
dc.identifier.issn | 0197-0186 | - |
dc.identifier.issn | 1872-9754 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/24681 | - |
dc.description.abstract | Opening of the mitochondrial permeability transition pore has been recognized to be involved in cell death. The present study investigated the effect of trifluoperazine and W-7 on the MPP+-induced mitochondrial damage and cell death in undifferentiated PC12 cells. Calmodulin antagonists (trifluoperazine, W-7 and calmidazolium) at 0.5-1 muM significantly reduced the loss of cell viability in PC12 cells treated with 500 muM MPP+. Trifluoperazine and W-7 (0.5-1 muM) inhibited the nuclear damage, the loss of the mitochondrial transmembrane potential followed by cytochrome c release, and the elevation of intracellular Ca2+ levels due to MPP+ in PC12 cells and attenuated the formation of reactive oxygen species and the depletion of GSH. Calmodulin antagonists at 5-10 muM exhibited a cytotoxic effect on PC12 cells, and compounds at 10 muM did not attenuate cytotoxicity of MPP+. Calmodulin antagonists (0.5-1 muM) significantly reduced rotenone-induced mitochondrial damage and cell death, whereas they did not attenuate cell death and elevation of intracellular Ca2+ levels due to H2O2 or ionomycin. The results show that trifluoperazine and W-7 exhibit a differential inhibitory effect against cytotoxicity of MPP+ depending on concentration. Both compounds at the concentrations less than 5 muM may attenuate the MPP+-induced viability loss in PC12 cells by suppressing change in the mitochondrial membrane permeability and by lowering the intracellular Ca2+ levels. (C) 2004 Elsevier Ltd. All rights reserved. | - |
dc.format.extent | 10 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | - |
dc.title | Inhibition of MPP+-induced mitochondrial damage and cell death by trifluoperazine and W-7 in PC12 cells | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.neuint.2004.07.007 | - |
dc.identifier.bibliographicCitation | NEUROCHEMISTRY INTERNATIONAL, v.46, no.2, pp 169 - 178 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000226322900008 | - |
dc.identifier.scopusid | 2-s2.0-14544286409 | - |
dc.citation.endPage | 178 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 169 | - |
dc.citation.title | NEUROCHEMISTRY INTERNATIONAL | - |
dc.citation.volume | 46 | - |
dc.type.docType | Article | - |
dc.publisher.location | 영국 | - |
dc.subject.keywordAuthor | trifluoperazine | - |
dc.subject.keywordAuthor | W-7 | - |
dc.subject.keywordAuthor | MPP+ | - |
dc.subject.keywordAuthor | mitochondrial membrane permeability | - |
dc.subject.keywordAuthor | apoptotic cell death | - |
dc.subject.keywordAuthor | PC12 cells | - |
dc.subject.keywordPlus | HYDROXYL RADICAL GENERATION | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | CYTOCHROME-C | - |
dc.subject.keywordPlus | MEMBRANE-PERMEABILITY | - |
dc.subject.keywordPlus | MPTP NEUROTOXICITY | - |
dc.subject.keywordPlus | BRAIN MITOCHONDRIA | - |
dc.subject.keywordPlus | CORTICAL-NEURONS | - |
dc.subject.keywordPlus | CALCIUM | - |
dc.subject.keywordPlus | CALMODULIN | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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