Activation of the Poly(ADP-Ribose) Polymerase Pathway in Human Heart Failure View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2006-07-30

AUTHORS

Andrea Molnár, Attila Tóth, Zsolt Bagi, Zoltán Papp, István Édes, Miklós Vaszily, Zoltán Galajda, Julius Gy. Papp, András Varró, Viktória Szüts, Zsombor Lacza, Domokos Gerö, Csaba Szabó

ABSTRACT

Poly(ADP-ribose) polymerase (PARP) activation has been implicated in the pathogenesis of acute and chronic myocardial dysfunction and heart failure. The goal of the present study was to investigate PARP activation in human heart failure, and to correlate PARP activation with various indices of apoptosis and oxidative and nitrosative stress in healthy (donor) and failing (NYHA class III–IV) human heart tissue samples. Higher levels of oxidized protein end-products were found in failing hearts compared with donor heart samples. On the other hand, no differences in tyrosine nitration (a marker of peroxynitrite generation) were detected. Activation of PARP was demonstrated in the failing hearts by an increased abundance of poly-ADP ribosylated proteins. Immunohistochemical analysis revealed that PARP activation was localized to the nucleus of the cardiomyocytes from the failing hearts. The expression of full-length PARP-1 was not significantly different in donor and failing hearts. The expression of caspase-9, in contrast, was significantly higher in the failing than in the donor hearts. Immunohistochemical analysis was used to detect the activation of mitochondrial apoptotic pathways. We found no significant translocation of apoptosis-inducing factor (AIF) into the nucleus. Overall, the current data provide evidence of oxidative stress and PARP activation in human heart failure. Interventional studies with antioxidants or PARP inhibitors are required to define the specific roles of these factors in the pathogenesis of human heart failure. More... »

PAGES

143-152

Identifiers

URI

http://scigraph.springernature.com/pub.10.2119/2006-00043.molnar

DOI

http://dx.doi.org/10.2119/2006-00043.molnar

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1068964945

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17088946


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28 schema:description Poly(ADP-ribose) polymerase (PARP) activation has been implicated in the pathogenesis of acute and chronic myocardial dysfunction and heart failure. The goal of the present study was to investigate PARP activation in human heart failure, and to correlate PARP activation with various indices of apoptosis and oxidative and nitrosative stress in healthy (donor) and failing (NYHA class III–IV) human heart tissue samples. Higher levels of oxidized protein end-products were found in failing hearts compared with donor heart samples. On the other hand, no differences in tyrosine nitration (a marker of peroxynitrite generation) were detected. Activation of PARP was demonstrated in the failing hearts by an increased abundance of poly-ADP ribosylated proteins. Immunohistochemical analysis revealed that PARP activation was localized to the nucleus of the cardiomyocytes from the failing hearts. The expression of full-length PARP-1 was not significantly different in donor and failing hearts. The expression of caspase-9, in contrast, was significantly higher in the failing than in the donor hearts. Immunohistochemical analysis was used to detect the activation of mitochondrial apoptotic pathways. We found no significant translocation of apoptosis-inducing factor (AIF) into the nucleus. Overall, the current data provide evidence of oxidative stress and PARP activation in human heart failure. Interventional studies with antioxidants or PARP inhibitors are required to define the specific roles of these factors in the pathogenesis of human heart failure.
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38 PARP inhibitors
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40 abundance
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43 analysis
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47 apoptotic pathway
48 cardiomyocytes
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51 contrast
52 current data
53 data
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55 donor heart samples
56 donor hearts
57 donors
58 dysfunction
59 evidence
60 expression
61 factors
62 failure
63 full-length PARP-1
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65 hand
66 heart
67 heart failure
68 heart samples
69 heart tissue samples
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71 human heart failure
72 human heart tissue samples
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