| Indices of apoptosis activation after blood cardioplegia and cardiopulmonary bypass. | |
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MedLine Citation:
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PMID: 16820582 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Cardioplegic arrest (CA) using cold blood cardioplegia (CBC) has been reported to reduce ischemia-reperfusion (IR)-induced myocardial injury via apoptosis. We studied key apoptotic mediators via the caspase-dependent and intrinsic pathways as well as poly(ADP)-ribosylating protein (PARP) activity in myocardial and peripheral tissues after CA and cardiopulmonary bypass (CBP). METHODS AND RESULTS: Right atrial (RA) and skeletal muscle(SM) was harvested from cardiac surgical patients with similar baseline characteristics (N =6) before and after CPB and CBC. Total and modified caspase-3, Bcl-2, Bad, apoptosis-inducing factor (AIF), and PARP were quantified by immunoblotting. Terminal caspase-3 activity was assessed and immunohistochemistry was performed for PARP and AIF. TUNEL staining was used for identification of apoptotic cells. Microarray gene expression analysis was performed using Affymetrix U95 GeneChip. In RA tissue, CA with CBC significantly increased phosphorylation of Bcl-2 (Ser70), Bad (Ser112) (2.63+/-0.4 and 1.77+/-0.3-fold respectively; P<0.05), and cleavage of the downstream caspase 3 (1.45+/-0.1-fold; P<0.05). There was no significant change in total protein levels. Also, there was an increase in mature AIF (57 kDa) levels (1.22+/-0.01-fold; P<0.05) and a trend toward nuclear translocation on histological staining. Caspase 3 activity was increased 1.5+/-0.14-fold (P<0.05). The number of apoptotic cells in atrial tissue increased after compared with before CPB/CA using TUNEL staining (1.55+/-0.66 versus 0.325+/-0.05%, respectively; P=0.03). In contrast, SM samples did not show any of the changes observed in RA tissue after CPB. CONCLUSIONS: Despite optimal current surgical myocardial protection, we found that CA with CBC induced both programmed cell death and survival signaling in myocardial tissue. |
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Authors:
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Basel Ramlawi; Jun Feng; Shigetoshi Mieno; Csaba Szabo; Zsuzsanna Zsengeller; Richard Clements; Neel Sodha; Munir Boodhwani; Cesario Bianchi; Frank W Sellke |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Circulation Volume: 114 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 2006 Jul |
Date Detail:
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Created Date: 2006-07-05 Completed Date: 2006-08-18 Revised Date: 2010-04-29 |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: United States |
Other Details:
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Languages: eng Pagination: I257-63 Citation Subset: AIM; IM |
Affiliation:
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Division of Cardiothoracic Surgery, Department of Surgery, Beth Israel Deaconess MedicalCenter, LMOB 2A, 110 Francis St, Boston, Massachusetts 02215, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aged Apoptosis* Apoptosis Inducing Factor / analysis Atrial Appendage / chemistry, pathology Blood* Cardiopulmonary Bypass / adverse effects* Caspase 3 Caspases / analysis Cell Hypoxia Female Gene Expression Profiling Heart Arrest, Induced / adverse effects, methods* Humans In Situ Nick-End Labeling Male Middle Aged Muscle Proteins / biosynthesis, genetics Muscle, Skeletal / chemistry, pathology Myocardial Reperfusion Oligonucleotide Array Sequence Analysis Oxidative Stress Phosphorylation Poly(ADP-ribose) Polymerases / analysis Protein Processing, Post-Translational Protein Transport Proto-Oncogene Proteins c-bcl-2 / analysis Tyrosine / analogs & derivatives, analysis bcl-Associated Death Protein / analysis |
| Grant Support | |
ID/Acronym/Agency:
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HL-46716/HL/NHLBI NIH HHS; HL-69024/HL/NHLBI NIH HHS; HL04095-06/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/AIFM1 protein, human; 0/Apoptosis Inducing Factor; 0/BAD protein, human; 0/Muscle Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-Associated Death Protein; 3604-79-3/3-nitrotyrosine; 55520-40-6/Tyrosine; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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