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

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dc.contributor.authorChoi, SE-
dc.contributor.authorMin, SH-
dc.contributor.authorShin, HC-
dc.contributor.authorKim, HE-
dc.contributor.authorJung, MW-
dc.contributor.authorKang, Y-
dc.date.accessioned2011-04-20T05:26:58Z-
dc.date.available2011-04-20T05:26:58Z-
dc.date.issued2006-
dc.identifier.issn0014-2999-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/2398-
dc.description.abstractReactive oxygen species are believed to be the central mediators of beta-cell destruction that leads to type 1 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 Ca(2+) plays a role in hydrogen peroxide (H(2)O(2))-induced MIN6N8a mouse beta cell death. Treatment with low concentration H(2)O(2) (50 microM) was found to be sufficient to reduce MIN6N8a cell viability by 55%, largely via apoptosis. However, this H(2)O(2)-induced cell death was near completely blocked by pretreatment with BAPTA/AM (5 microM), a chelator of intracellular Ca(2+). Moreover, the intracellular calcium store channel blockers, such as, xestospongin c and ryanodine, significant protected cells from 50 microM H(2)O(2)-induced cell death and under extracellular Ca(2+)-free conditions, 50 microM H(2)O(2) elicited transient [Ca(2+)](i) increases. In addition, pharmacologic inhibitors of calpain, calcineurin, and calcium/calmodulin-dependent protein kinase II were found to have a protective effect on H(2)O(2)-induced death. Moreover, H(2)O(2)-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 Ca(2+) chelation. These findings show that [Ca(2+)](i) elevation, possibly due to release from intracellular calcium stores and the subsequent activation of Ca(2+)-mediated apoptotic signals, critically mediates low concentration H(2)O(2)-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.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis-
dc.subject.MESHCalcineurin-
dc.subject.MESHCalcium-
dc.subject.MESHCalpain-
dc.subject.MESHCaspase 3-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHCell Survival-
dc.subject.MESHChelating Agents-
dc.subject.MESHEgtazic Acid-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHEnzyme Inhibitors-
dc.subject.MESHHydrogen Peroxide-
dc.subject.MESHInsulinoma-
dc.subject.MESHIntracellular Fluid-
dc.subject.MESHJNK Mitogen-Activated Protein Kinases-
dc.subject.MESHMacrocyclic Compounds-
dc.subject.MESHOxazoles-
dc.subject.MESHOxidants-
dc.subject.MESHPoly(ADP-ribose) Polymerases-
dc.subject.MESHRyanodine-
dc.subject.MESHSignal Transduction-
dc.titleInvolvement of calcium-mediated apoptotic signals in H2O2-induced MIN6N8a cell death.-
dc.typeArticle-
dc.identifier.pmid16934799-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0014-2999(06)00639-X-
dc.contributor.affiliatedAuthor최, 성이-
dc.contributor.affiliatedAuthor정, 민환-
dc.contributor.affiliatedAuthor강, 엽-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.ejphar.2006.06.016-
dc.citation.titleEuropean journal of pharmacology-
dc.citation.volume547-
dc.citation.number1-3-
dc.citation.date2006-
dc.citation.startPage1-
dc.citation.endPage9-
dc.identifier.bibliographicCitationEuropean journal of pharmacology, 547(1-3). : 1-9, 2006-
dc.identifier.eissn1879-0712-
dc.relation.journalidJ000142999-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
Journal Papers > Research Organization > Institute for Medical Sciences
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