Mechanisms of apoptosis after ischemia and reperfusion: Role of the renin-angiotensin system
Abstract Background: Apoptosis plays a key role in the pathogenesis of cardiac diseases. We examined the influence of the renin-angiotensin system (RAS) on different regulators of apoptosis using an isolated hemoperfused working porcine heart model of acute ischemia (2 h), followed by reperfusion (4 h). Methods and Results: 23 porcine hearts were randomized to 5 groups: hemoperfused non-infarcted hearts (C), infarcted hearts (MI: R. circumflexus), infarcted hearts treated with quinaprilat (Q), infarcted hearts treated with angiotensin-I (Ang I), and infarcted hearts treated with angiotensin-I and quinaprilat (QA). Fas, Bax, bcl-2 and p53 proteins were increased in MI hearts and further elevated by Ang I. Quinaprilat reduced Bax and p53. Bcl-2 was elevated in Q and reduced in QA. An early upregulation of caspase-3 gene and protein expression was detected in MI and Ang I hearts compared to C. Q reduced caspase-3 gene expression, but had no effect on caspase-3 and Fas protein. Conclusions: These data suggest that the RAS plays a pivotal role in cardiac apoptosis which is the early and predominant form of death in myocardial infarction. Ischemia/reperfusion induces programmed cell death via extrinsic and intrinsic pathways. Early treatment with quinaprilat attenuated cardiomyocyte apoptosis..
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2006 |
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Erschienen: |
2006 |
Enthalten in: |
Zur Gesamtaufnahme - volume:11 |
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Enthalten in: |
Apoptosis - 11(2006), 3 vom: März, Seite 347-358 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Kossmehl, P. [VerfasserIn] |
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Links: |
Volltext [lizenzpflichtig] |
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Anmerkungen: |
© Springer Science + Business Media, Inc. 2006 |
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doi: |
10.1007/s10495-006-4350-9 |
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funding: |
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PPN (Katalog-ID): |
OLC2111321311 |
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520 | |a Abstract Background: Apoptosis plays a key role in the pathogenesis of cardiac diseases. We examined the influence of the renin-angiotensin system (RAS) on different regulators of apoptosis using an isolated hemoperfused working porcine heart model of acute ischemia (2 h), followed by reperfusion (4 h). Methods and Results: 23 porcine hearts were randomized to 5 groups: hemoperfused non-infarcted hearts (C), infarcted hearts (MI: R. circumflexus), infarcted hearts treated with quinaprilat (Q), infarcted hearts treated with angiotensin-I (Ang I), and infarcted hearts treated with angiotensin-I and quinaprilat (QA). Fas, Bax, bcl-2 and p53 proteins were increased in MI hearts and further elevated by Ang I. Quinaprilat reduced Bax and p53. Bcl-2 was elevated in Q and reduced in QA. An early upregulation of caspase-3 gene and protein expression was detected in MI and Ang I hearts compared to C. Q reduced caspase-3 gene expression, but had no effect on caspase-3 and Fas protein. Conclusions: These data suggest that the RAS plays a pivotal role in cardiac apoptosis which is the early and predominant form of death in myocardial infarction. Ischemia/reperfusion induces programmed cell death via extrinsic and intrinsic pathways. Early treatment with quinaprilat attenuated cardiomyocyte apoptosis. | ||
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700 | 1 | |a Kurth, E. |4 aut | |
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700 | 1 | |a Wehland, M. |4 aut | |
700 | 1 | |a Kreutz, R. |4 aut | |
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700 | 1 | |a J. Danser, A. H. |4 aut | |
700 | 1 | |a Grosse, J. |4 aut | |
700 | 1 | |a Paul, M. |4 aut | |
700 | 1 | |a Grimm, D. |4 aut | |
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