pubmed-article:21185334 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21185334 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
pubmed-article:21185334 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
pubmed-article:21185334 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
pubmed-article:21185334 | lifeskim:mentions | umls-concept:C0085403 | lld:lifeskim |
pubmed-article:21185334 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
pubmed-article:21185334 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:21185334 | pubmed:dateCreated | 2011-6-6 | lld:pubmed |
pubmed-article:21185334 | pubmed:abstractText | To clarify the relationship between reactive oxygen species (ROS) and cell death during ischemia-reperfusion (I/R), we studied cell death mechanisms in a cellular model of I/R. Oxidant stress during simulated ischemia was detected in the mitochondrial matrix using mito-roGFP, a ratiometric redox sensor, and by Mito-Sox Red oxidation. Reperfusion-induced death was attenuated by over-expression of Mn-superoxide dismutase (Mn-SOD) or mitochondrial phospholipid hydroperoxide glutathione peroxidase (mito-PHGPx), but not by catalase, mitochondria-targeted catalase, or Cu,Zn-SOD. Protection was also conferred by chemically distinct antioxidant compounds, and mito-roGFP oxidation was attenuated by NAC, or by scavenging of residual O(2) during the ischemia (anoxic ischemia). Mitochondrial permeability transition pore (mPTP) oscillation/opening was monitored by real-time imaging of mitochondrial calcein fluorescence. Oxidant stress caused release of calcein to the cytosol during ischemia, a response that was inhibited by chemically diverse antioxidants, anoxia, or over-expression of Mn-SOD or mito-PHGPx. These findings suggest that mitochondrial oxidant stress causes oscillation of the mPTP prior to reperfusion. Cytochrome c release from mitochondria to the cytosol was not detected until after reperfusion, and was inhibited by anoxic ischemia or antioxidant administration during ischemia. Although DNA fragmentation was detected after I/R, no evidence of Bax activation was detected. Over-expression of the anti-apoptotic protein Bcl-X(L) in cardiomyocytes did not confer protection against I/R-induced cell death. Moreover, murine embryonic fibroblasts with genetic depletion of Bax and Bak, or over-expression of Bcl-X(L), failed to show protection against I/R. These findings indicate that mitochondrial ROS during ischemia triggers mPTP activation, mitochondrial depolarization, and cell death during reperfusion through a Bax/Bak-independent cell death pathway. Therefore, mitochondrial apoptosis appears to represent a redundant death pathway in this model of simulated I/R. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection. | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:language | eng | lld:pubmed |
pubmed-article:21185334 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21185334 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:21185334 | pubmed:month | Jul | lld:pubmed |
pubmed-article:21185334 | pubmed:issn | 0006-3002 | lld:pubmed |
pubmed-article:21185334 | pubmed:author | pubmed-author:ChandelNavdee... | lld:pubmed |
pubmed-article:21185334 | pubmed:author | pubmed-author:Vanden... | lld:pubmed |
pubmed-article:21185334 | pubmed:author | pubmed-author:SchumackerPau... | lld:pubmed |
pubmed-article:21185334 | pubmed:author | pubmed-author:IwaseHirotaro... | lld:pubmed |
pubmed-article:21185334 | pubmed:author | pubmed-author:WaypaGregory... | lld:pubmed |
pubmed-article:21185334 | pubmed:author | pubmed-author:KondapalliJyo... | lld:pubmed |
pubmed-article:21185334 | pubmed:author | pubmed-author:GuzyRobert... | lld:pubmed |
pubmed-article:21185334 | pubmed:author | pubmed-author:LoorGabrielG | lld:pubmed |
pubmed-article:21185334 | pubmed:copyrightInfo | Copyright © 2010 Elsevier B.V. All rights reserved. | lld:pubmed |
pubmed-article:21185334 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:21185334 | pubmed:volume | 1813 | lld:pubmed |
pubmed-article:21185334 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:21185334 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:21185334 | pubmed:pagination | 1382-94 | lld:pubmed |
pubmed-article:21185334 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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pubmed-article:21185334 | pubmed:year | 2011 | lld:pubmed |
pubmed-article:21185334 | pubmed:articleTitle | Mitochondrial oxidant stress triggers cell death in simulated ischemia-reperfusion. | lld:pubmed |
pubmed-article:21185334 | pubmed:affiliation | Department of Surgery, University of Chicago, Chicago, IL 60637, USA. | lld:pubmed |
pubmed-article:21185334 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:21185334 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:21185334 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |