| Spatial variability in T-tubule and electrical remodeling of left ventricular epicardium in mouse hearts with transgenic Gαq overexpression-induced pathological hypertrophy. | |
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MedLine Citation:
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PMID: 22728217 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Pathological left ventricular hypertrophy (LVH) is consistently associated with prolongation of the ventricular action potentials. A number of previous studies, employing various experimental models of hypertrophy, have revealed marked differences in the effects of hypertrophy on action potential duration (APD) between myocytes from endocardial and epicardial layers of the LV free wall. It is not known, however, whether pathological LVH is also accompanied by redistribution of APD among myocytes from the same layer in the LV free wall. In the experiments here, LV epicardial action potential remodeling was examined in a mouse model of decompensated LVH, produced by cardiac-restricted transgenic Gαq overexpression. Confocal linescanning-based optical recordings of propagated action potentials from individual in situ cardiomyocytes across the outer layer of the anterior LV epicardium demonstrated spatially non-uniform action potential prolongation in transgenic hearts, giving rise to alterations in spatial dispersion of epicardial repolarization. Local density and distribution of anti-Cx43 mmune reactivity in Gαq hearts were unchanged compared to wild-type hearts, suggesting preservation of intercellular coupling. Confocal microscopy also revealed heterogeneous disorganization of T-tubules in epicardial cardiomyocytes in situ. These data provide evidence of the existence of significant electrical and structural heterogeneity within the LV epicardial layer of hearts with transgenic Gαq overexpression-induced hypertrophy, and further support the notion that a small portion of electrically well connected LV tissue can maintain dispersion of action potential duration through heterogeneity in the activities of sarcolemmal ionic currents that control repolarization. It remains to be examined whether other experimental models of pathological LVH, including pressure overload LVH, similarly exhibit alterations in T-tubule organization and/or dispersion of repolarization within distinct layers of LV myocardium. |
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Authors:
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Wen Tao; Jianjian Shi; Gerald W Dorn; Lei Wei; Michael Rubart |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2012-06-21 |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 53 ISSN: 1095-8584 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2012 Sep |
Date Detail:
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Created Date: 2012-08-13 Completed Date: 2012-12-17 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 409-19 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Ltd. All rights reserved. |
Affiliation:
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Riley Heart Research Center, Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202-5225, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials Animals Connexin 43 / genetics, metabolism GTP-Binding Protein alpha Subunits, Gq-G11 / genetics* Gene Expression* Hypertrophy, Left Ventricular / genetics*, physiopathology* Mice Mice, Transgenic Myocardium / metabolism, ultrastructure Pericardium / metabolism*, physiopathology* Ventricular Remodeling / genetics* |
| Grant Support | |
ID/Acronym/Agency:
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P01 HL085098/HL/NHLBI NIH HHS; P01HL085098/HL/NHLBI NIH HHS; R01 HL075165/HL/NHLBI NIH HHS; R01HL075165/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Connexin 43; EC 3.6.5.1/GTP-Binding Protein alpha Subunits, Gq-G11 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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