Involvement of calcium-mediated apoptotic signals in H2O2-induced MIN6N8a cell death

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dc.contributor.authorChoi, SEko
dc.contributor.authorMin, SHko
dc.contributor.authorShin, HCko
dc.contributor.authorKim, HEko
dc.contributor.authorJung, MWko
dc.contributor.authorKang, Yko
dc.date.accessioned2013-03-08T14:17:43Z-
dc.date.available2013-03-08T14:17:43Z-
dc.date.created2013-02-20-
dc.date.created2013-02-20-
dc.date.issued2006-10-
dc.identifier.citationEUROPEAN JOURNAL OF PHARMACOLOGY, v.547, pp.1 - 9-
dc.identifier.issn0014-2999-
dc.identifier.urihttp://hdl.handle.net/10203/93235-
dc.description.abstractReactive oxygen species are believed to be the central mediators of beta-cell destruction that leads to type I and 2 diabetes, and calcium has been reported to be an important mediator of beta cell death. In the present study, the authors investigated whether Ca2+ plays a role in hydrogen peroxide (H2O2)-induced MIN6N8a mouse beta cell death. Treatment with low concentration H2O2 (50 mu M) was found to be sufficient to reduce MIN6N8a cell viability by 55%, largely via apoptosis. However, this H2O2-induced cell death was near completely blocked by pretreatment with BAPTA/AM (5 mu M), a chelator of intracellular Ca2+ Moreover, the intracellular calcium store channel blockers, such as, xestospongin c and ryanodine, significant protected cells from 50 mu M H2O2-induced cell death and under extracellular Ca2+-free conditions, 50 mu M H2O2 elicited transient [Ca2+](i) increases. In addition, pharmacologic inhibitors of calpain, calcineurin, and calcium/calmodulin-dependent protein kinase 11 were found to have a protective effect on H2O2-induced death. Moreover, H2O2-induced apoptotic signals, such as c-JUN N-terminal kinase activation, cytochrome c release, caspase 3 activation, and poly (ADP-ribose) polymerase cleavage were all down-regulated by the intracellular Ca2+ chelation. These findings show that [Ca2+](i) elevation, possibly due to release from intracellular calcium stores and the subsequent activation of Ca2+-mediated apoptotic signals, critically mediates low concentration H2O2-induced MIN6N8a cell death. These findings suggest that a breakdown of calcium homeostasis by low level of reactive oxygen species may be involved in beta cell destruction during diabetes development. (c) 2006 Published by Elsevier B.V.-
dc.languageEnglish-
dc.publisherELSEVIER SCIENCE BV-
dc.subjectPANCREATIC BETA-CELLS-
dc.subjectOXIDATIVE STRESS-
dc.subjectHYDROGEN-PEROXIDE-
dc.subjectPERMEABILITY TRANSITION-
dc.subjectPROTEIN-KINASES-
dc.subjectCA2+ INFLUX-
dc.subjectIN-VITRO-
dc.subjectMITOCHONDRIAL-
dc.subjectACTIVATION-
dc.subjectEXPRESSION-
dc.titleInvolvement of calcium-mediated apoptotic signals in H2O2-induced MIN6N8a cell death-
dc.typeArticle-
dc.identifier.wosid000241172400001-
dc.identifier.scopusid2-s2.0-33748559475-
dc.type.rimsART-
dc.citation.volume547-
dc.citation.beginningpage1-
dc.citation.endingpage9-
dc.citation.publicationnameEUROPEAN JOURNAL OF PHARMACOLOGY-
dc.identifier.doi10.1016/j.ejphar.2006.06.016-
dc.contributor.localauthorJung, MW-
dc.contributor.nonIdAuthorChoi, SE-
dc.contributor.nonIdAuthorMin, SH-
dc.contributor.nonIdAuthorShin, HC-
dc.contributor.nonIdAuthorKim, HE-
dc.contributor.nonIdAuthorKang, Y-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorBAPTA/AM [1,2-bis(o-aminophenoxy)ethane-N,N,N&apos-
dc.subject.keywordAuthor,N&apos-
dc.subject.keywordAuthortetraacetic acid/tetra(acetoxymethyl) ester]-
dc.subject.keywordAuthorbeta cell-
dc.subject.keywordAuthorCa2+[calcium]-
dc.subject.keywordAuthorH2O2 [hydrogen peroxide]-
dc.subject.keywordPlusPANCREATIC BETA-CELLS-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusHYDROGEN-PEROXIDE-
dc.subject.keywordPlusPERMEABILITY TRANSITION-
dc.subject.keywordPlusPROTEIN-KINASES-
dc.subject.keywordPlusCA2+ INFLUX-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusMITOCHONDRIAL-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusEXPRESSION-
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