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pubmed, article, google, scholar, cas, mitochondrial, mitochondria, central, injury, zazueta, caveolin, cardiac, res, patel, erk, heart, cell, physiol, méxico, basic, signaling, ischemiareperfusion, caveolae, function, cardioprotective, correa, postconditioning, reperfusion, cardiol, doi, roth, subsarcolemmal, garcíaniño, subpopulations, access, dois, mol, privacy, cookies, content, research, hearts, postc, cardioprotection, wang, circ, oxidative, biochem, membrane, protein,

Topics {✒️}

mabel buelna-chontal wylly ramsés garcía-niño juan carlos león-contreras methyl-β-cyclodextrin abolished cardioprotection diminished pho-erk1/2 gold-labeling author information authors article garcía-niño month download article/chapter redox-sensitive mitochondrial phosphorylation/translocation myocardial ischemia/reperfusion injury activating mek/erk1/2 signaling methyl-β-cyclodextrin abolished rogelio hernández-pando cecilia zazueta phosphorylated erk/map kinases pkcepsilon-induced cardioprotection mitochondrial erk1/2 activation cardiac mitochondrial subpopulations time-lapse confocal microscopy article basic research oxidative stress-induced injury elizabeth soria-castro alpha-linolenic acid protects isoflurane-induced cardiac protection julia isabel rodríguez-barrena mitochondrial dysfunction due caveolin-rich membrane domains full article pdf related subjects ciudad de méxico open mitokatp channels hypertensive dilated cardiomyopathy permeability transition pore mitochondrial subpopulations ischemia/reperfusion injury differential mapk activation vega-garcía cc pho-erk1/2 interaction cardioprotective signaling driven cardioprotective kinase signaling check access instant access privacy choices/manage cookies mitochondrial calcium transport ruíz-de-jesús facultad de química ruiz-meana heart induces formation rat cardiac mitochondrial ischemia time impacts

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         headline:Cardioprotective kinase signaling to subsarcolemmal and interfibrillar mitochondria is mediated by caveolar structures
         description:The demonstration that caveolin-3 overexpression reduces myocardial ischemia/reperfusion injury and our own finding that multiprotein signaling complexes increase in mitochondria in association with caveolin-3 levels, led us to investigate the contribution of caveolae-driven extracellular signal-regulated kinases 1/2 (ERK1/2) on maintaining the function of cardiac mitochondrial subpopulations from reperfused hearts subjected to postconditioning (PostC). Rat hearts were isolated and subjected to ischemia/reperfusion and to PostC. Enhanced cardiac function, reduced infarct size and preserved ultrastructure of cardiomyocytes were associated with increased formation of caveolar structures, augmented levels of caveolin-3 and mitochondrial ERK1/2 activation in PostC hearts in both subsarcolemmal (SSM) and interfibrillar (IFM) subpopulations. Disruption of caveolae with methyl-β-cyclodextrin abolished cardioprotection in PostC hearts and diminished pho-ERK1/2 gold-labeling in both mitochondrial subpopulations in correlation with suppression of resistance to permeability transition pore opening. Also, differences between the mitochondrial subpopulations in the setting of PostC were evaluated. Caveolae disruption with methyl-β-cyclodextrin abolished the cardioprotective effect of postconditioning by inhibiting the interaction of ERK1/2 with mitochondria and promoted decline in mitochondrial function. SSM, which are particularly sensitive to reperfusion damage, take advantage of their location in cardiomyocyte boundary and benefit from the cardioprotective signaling driven by caveolae, avoiding injury propagation.
         datePublished:2017-02-03T00:00:00Z
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            Postconditioning
            Mitochondrial subpopulations
            Caveolae
            Mitochondrial ERK1/2
            Cardiology
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      headline:Cardioprotective kinase signaling to subsarcolemmal and interfibrillar mitochondria is mediated by caveolar structures
      description:The demonstration that caveolin-3 overexpression reduces myocardial ischemia/reperfusion injury and our own finding that multiprotein signaling complexes increase in mitochondria in association with caveolin-3 levels, led us to investigate the contribution of caveolae-driven extracellular signal-regulated kinases 1/2 (ERK1/2) on maintaining the function of cardiac mitochondrial subpopulations from reperfused hearts subjected to postconditioning (PostC). Rat hearts were isolated and subjected to ischemia/reperfusion and to PostC. Enhanced cardiac function, reduced infarct size and preserved ultrastructure of cardiomyocytes were associated with increased formation of caveolar structures, augmented levels of caveolin-3 and mitochondrial ERK1/2 activation in PostC hearts in both subsarcolemmal (SSM) and interfibrillar (IFM) subpopulations. Disruption of caveolae with methyl-β-cyclodextrin abolished cardioprotection in PostC hearts and diminished pho-ERK1/2 gold-labeling in both mitochondrial subpopulations in correlation with suppression of resistance to permeability transition pore opening. Also, differences between the mitochondrial subpopulations in the setting of PostC were evaluated. Caveolae disruption with methyl-β-cyclodextrin abolished the cardioprotective effect of postconditioning by inhibiting the interaction of ERK1/2 with mitochondria and promoted decline in mitochondrial function. SSM, which are particularly sensitive to reperfusion damage, take advantage of their location in cardiomyocyte boundary and benefit from the cardioprotective signaling driven by caveolae, avoiding injury propagation.
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      dateModified:2017-02-03T00:00:00Z
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      pageEnd:15
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         Cardioprotection
         Postconditioning
         Mitochondrial subpopulations
         Caveolae
         Mitochondrial ERK1/2
         Cardiology
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