| Upregulation of Bcl-2 proteins during the transition to pressure overload-induced heart failure. | |
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MedLine Citation:
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PMID: 17112608 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Cardiomyocyte apoptosis is implicated in the pathogenesis of heart failure and mitochondria play an important role in this mode of cell death. In this study, activity of the Bcl-2 family of mitochondrial apoptotic proteins and their regulator (p53) were assessed during the transition to heart failure. METHODS: Ten adult male sheep were banded with a variable aortic constriction device. This was progressively inflated to increase left ventricular (LV) afterload. The sheep were monitored echocardiographically, measuring LV Mass Index (LVMI), diastolic LV Internal Diameter (LVIDd) and Fractional Shortening (FS). Serial LV endomyocardial biopsies were obtained, to measure expression of p53 and Bcl-2 family proteins by Western blotting. RESULTS: Over the first 3-4 weeks, the sheep developed hypertrophy (LVMI 79.5+/-4.6 vs. 44.0+/-3.0 g/m2, p<0.01), followed by gradual LV dilatation (LVIDd 4.23+/-0.08 vs. 3.39+/-0.07 cm, p<0.01). Ventricular function remained stable until 7-8 weeks post banding, when there was significant deterioration (FS 18.3+/-2.4 vs. 46.9+/-2.6%, p<0.01), associated with clinical heart failure. Upregulation of the Bax/Bcl-2 ratio, associated with increased levels of p53, was demonstrated in each of the echocardiographically defined stages (LV hypertrophy, LV dilatation and LV failure). In parallel, significantly higher levels of anti-apoptotic protein (Bcl-xL) was associated with LV dilatation and failure. CONCLUSIONS: Upregulation of Bax/Bcl-2 ratio occurs during the transition to heart failure and in particular with the initial hypertrophic response. Increase in expression of the anti-apoptotic protein Bcl-xL suggests possible concomitant compensatory mechanisms being activated during the transition to heart failure. |
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Authors:
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Narain Moorjani; Pedro Catarino; Danyah Trabzuni; Soad Saleh; Azad Moorji; Nduna Dzimiri; Futwan Al-Mohanna; Stephen Westaby; Manzoor Ahmad |
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Publication Detail:
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Type: Comparative Study; Journal Article Date: 2006-11-16 |
Journal Detail:
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Title: International journal of cardiology Volume: 116 ISSN: 1874-1754 ISO Abbreviation: Int. J. Cardiol. Publication Date: 2007 Mar |
Date Detail:
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Created Date: 2007-02-16 Completed Date: 2007-04-09 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8200291 Medline TA: Int J Cardiol Country: Netherlands |
Other Details:
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Languages: eng Pagination: 27-33 Citation Subset: IM |
Affiliation:
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Department of Cardiothoracic Surgery, Oxford Heart Centre, John Radcliffe Hospital, Oxford OX3 9DY, United Kingdom. narain.moorjani@doctors.org.uk |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Disease Models, Animal Heart Failure / complications, metabolism*, pathology Heart Ventricles / ultrasonography Male Myocardium / pathology Proto-Oncogene Proteins c-bcl-2 / metabolism* Reference Values Sheep Tumor Suppressor Protein p53 / metabolism Ventricular Dysfunction, Left / etiology, metabolism Ventricular Pressure |
| Chemical | |
Reg. No./Substance:
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0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Suppressor Protein p53 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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