Postconditioning induces an anti-apoptotic effect and preserves mitochondrial integrity in isolated rat hearts

Penna, Cláudia; Perrelli, Maria-Giulia; Raimondo, Stefania; Tullio, Francesca; Merlino, Annalisa; Moro, Francesca; Geuna, Stefano; Mancardi, Daniele; Pagliaro, Pasquale

doi:10.1016/j.bbabio.2009.03.013

Cited by 66 publications

(96 citation statements)

References 59 publications

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“…The methods were similar to those previously described [45,[50][51][52][53][54]. In brief, each animal was anesthetized.…”

Section: Isolated Heart Perfusionmentioning

confidence: 99%

“…Pacing was discontinued on initiation of ischemia and restarted after the 3 rd minute of reperfusion in all groups [44,[50][51][52][53][54]. After stabilization, the hearts of the Control group (I/R, Group 1, n=12) were exposed to 30-min ischemia and then to 120-min reperfusion only.…”

Section: Experimental Protocols (Fig 2)mentioning

confidence: 99%

“…In Group 2 (PostC group; n=12) after the 30-min ischemia the hearts immediately underwent a protocol of PostC (i.e. five cycles of 10-s reperfusion and ischemia) [50][51][52][53][54].…”

Section: Experimental Protocols (Fig 2)mentioning

confidence: 99%

“…The homogenate was centrifuged at 4 °C for 30-min at 13,000 g, and the supernatant was collected to quantify proteins with Bradford's method [5]. Western blot analyses were performed as previously described [53].…”

Section: Cat and Sod Levels By Western Blot Analysismentioning

confidence: 99%

“…Therefore, it is likely that interplays between redox and acid/base conditions in early reperfusion exist. Clearly the PostC cycles (i.e., intermittent re-oxygenation) and the early acidosis may be responsible of modifications of enzyme activities and chemical reactions, which lead to produce a few ROS with signaling role instead of ROS stress [13,51,53].…”

Section: Introductionmentioning

confidence: 99%

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Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Penna

Perrelli

Tullio

et al. 2011

Pflugers Arch - Eur J Physiol

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Postconditioning (PostC) modifies early post-ischemic pH, redox-environment and activity of enzymes. We hypothesized that early acidosis in PostC may affect superoxide-dismutase (SOD) and catalase(CAT) activities, may reduce 3-nitrotyrosine(3-NT)-and may increase S-nitrosylated (SNO)-protein levels, thus deploying its protective effects. To verify this hypothesis, we studied early (7 th min) and late (120 th min) phases of reperfusion a) endogenous-SOD and -CAT activities, and b) 3-NT-and SNO-protein levels. Isolated rat hearts underwent 30-min ischemia/120-min reperfusion(I/R) or PostC (5 cycles of 10-s I/R at the beginning of 120-min reperfusion) either with or without exogenous-CAT or -SOD infused during the initial 3-min of reperfusion. The effects of early reperfusion with acidic-buffer(AB, pH 6.8) on endogenous antioxidant-enzymes were also tested. Pressure, infarct-size and lactate-dehydrogenase release were also measured. At the 7 th min, PostC induced a significant decrease in SOD-activity with no major change in both Mn-and Cu/Zn-SOD levels, and in CAT-activity and level. PostC also reduced 3-NT and increased SNO levels. Exogenous-SOD, but not -CAT abolished PostCcardioprotection. In late reperfusion(120-min), I/R increased SOD-activity, but decreased CATactivity and Cu/Zn-SOD levels; these effects were reversed by PostC; 3-NT was not affected, but SNO was increased by PostC. AB reproduced PostC effects on antioxidant-enzymes.Conclusions: PostC downregulates endogenous-SOD and preserves -CAT activity, thus increasing SNO and reducing 3-NT levels. These effects are triggered by early post-ischemic acidosis. Yet acidosis-induced SOD-downregulation may limit denitrosylation; thus contributing to PostC-triggering. Hence, exogenous-SOD, but not -CAT, interferes with PostC-triggering.Persistent SOD-downregulation and SNO-increase may contribute to PostC and AB beneficial effects.

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“…The methods were similar to those previously described [45,[50][51][52][53][54]. In brief, each animal was anesthetized.…”

Section: Isolated Heart Perfusionmentioning

confidence: 99%

Section: Experimental Protocols (Fig 2)mentioning

confidence: 99%

“…In Group 2 (PostC group; n=12) after the 30-min ischemia the hearts immediately underwent a protocol of PostC (i.e. five cycles of 10-s reperfusion and ischemia) [50][51][52][53][54].…”

Section: Experimental Protocols (Fig 2)mentioning

confidence: 99%

Section: Cat and Sod Levels By Western Blot Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Penna

Perrelli

Tullio

et al. 2011

Pflugers Arch - Eur J Physiol

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Connexin 43 and Mitochondria in Cardiovascular Health and Disease

Boengler

Schulz

2017

Advances in Experimental Medicine and Biology

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Connexin 43 (Cx43) is the major connexin protein in ventricular cardiomyocytes. Six Cx43 proteins assemble into so-called hemichannels at the sarcolemma and opposing hemichannels form gap junctions, which allow the passage of small molecules and electrical current flow between adjacent cells. Apart from its localization at the plasma membrane, Cx43 is also present in cardiomyocyte mitochondria, where it is important for mitochondrial function in terms of oxygen consumption and potassium fluxes. The expression of gap junctional and mitochondrial Cx43 is altered under several pathophysiological conditions among them are hypertension, hypertrophy, hypercholesterolemia, ischemia/reperfusion injury, post-infarction remodeling, and heart failure. The present review will focus on the role of Cx43 in cardiovascular diseases and will highlight the importance of mitochondrial Cx43 in cardioprotection.

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Reactive Oxygen Species (ROS) and Cardiac Ischemia and Reperfusion Injury

Camara

Stowe

2014

Systems Biology of Free Radicals and Antioxidants

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Postconditioning induces an anti-apoptotic effect and preserves mitochondrial integrity in isolated rat hearts

Cited by 66 publications

References 59 publications

Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Connexin 43 and Mitochondria in Cardiovascular Health and Disease

Reactive Oxygen Species (ROS) and Cardiac Ischemia and Reperfusion Injury

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