DC Field | Value | Language |
---|---|---|
dc.contributor.author | Choi, SE | ko |
dc.contributor.author | Min, SH | ko |
dc.contributor.author | Shin, HC | ko |
dc.contributor.author | Kim, HE | ko |
dc.contributor.author | Jung, MW | ko |
dc.contributor.author | Kang, Y | ko |
dc.date.accessioned | 2013-03-08T14:17:43Z | - |
dc.date.available | 2013-03-08T14:17:43Z | - |
dc.date.created | 2013-02-20 | - |
dc.date.created | 2013-02-20 | - |
dc.date.issued | 2006-10 | - |
dc.identifier.citation | EUROPEAN JOURNAL OF PHARMACOLOGY, v.547, pp.1 - 9 | - |
dc.identifier.issn | 0014-2999 | - |
dc.identifier.uri | http://hdl.handle.net/10203/93235 | - |
dc.description.abstract | Reactive 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.language | English | - |
dc.publisher | ELSEVIER SCIENCE BV | - |
dc.subject | PANCREATIC BETA-CELLS | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | HYDROGEN-PEROXIDE | - |
dc.subject | PERMEABILITY TRANSITION | - |
dc.subject | PROTEIN-KINASES | - |
dc.subject | CA2+ INFLUX | - |
dc.subject | IN-VITRO | - |
dc.subject | MITOCHONDRIAL | - |
dc.subject | ACTIVATION | - |
dc.subject | EXPRESSION | - |
dc.title | Involvement of calcium-mediated apoptotic signals in H2O2-induced MIN6N8a cell death | - |
dc.type | Article | - |
dc.identifier.wosid | 000241172400001 | - |
dc.identifier.scopusid | 2-s2.0-33748559475 | - |
dc.type.rims | ART | - |
dc.citation.volume | 547 | - |
dc.citation.beginningpage | 1 | - |
dc.citation.endingpage | 9 | - |
dc.citation.publicationname | EUROPEAN JOURNAL OF PHARMACOLOGY | - |
dc.identifier.doi | 10.1016/j.ejphar.2006.06.016 | - |
dc.contributor.localauthor | Jung, MW | - |
dc.contributor.nonIdAuthor | Choi, SE | - |
dc.contributor.nonIdAuthor | Min, SH | - |
dc.contributor.nonIdAuthor | Shin, HC | - |
dc.contributor.nonIdAuthor | Kim, HE | - |
dc.contributor.nonIdAuthor | Kang, Y | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | BAPTA/AM [1,2-bis(o-aminophenoxy)ethane-N,N,N&apos | - |
dc.subject.keywordAuthor | ,N&apos | - |
dc.subject.keywordAuthor | tetraacetic acid/tetra(acetoxymethyl) ester] | - |
dc.subject.keywordAuthor | beta cell | - |
dc.subject.keywordAuthor | Ca2+[calcium] | - |
dc.subject.keywordAuthor | H2O2 [hydrogen peroxide] | - |
dc.subject.keywordPlus | PANCREATIC BETA-CELLS | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | HYDROGEN-PEROXIDE | - |
dc.subject.keywordPlus | PERMEABILITY TRANSITION | - |
dc.subject.keywordPlus | PROTEIN-KINASES | - |
dc.subject.keywordPlus | CA2+ INFLUX | - |
dc.subject.keywordPlus | IN-VITRO | - |
dc.subject.keywordPlus | MITOCHONDRIAL | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
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