Document Detail


Uncoupling between enhanced excitation-contraction coupling and the response to heart disease: Lessons from the PI3K gamma knockout murine model.
MedLine Citation:
PMID:  21276799     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The heart is a mechanosensitive organ that adapts its morphology to changing hemodynamic conditions via a process named mechanotransduction, which is the primary means of detecting mechanical stress in the extracellular environment. In the heart, mechanical signals are propagated into the intracellular space primarily via cell-adhesion complexes and are subsequently transmitted from cell to cell via paracrine signaling. Enhanced excitation-contraction coupling increases myocardial contractility in various experimental models. However, these animal models routinely show increased susceptibility to biomechanical stress with the development of early ventricular dilation and reduced systolic function in the setting of adverse myocardial remodeling. The enhanced susceptibility of the PI3Kγ knockout mice to biomechanical stress is linked to a cAMP-dependent upregulation of matrix metalloproteinase with a loss of N-cadherin mediated cell adhesion. Enhancing cell-cell adhesion and cell-ECM interaction will promote the salutary effects of enhanced intracellular Ca(2+) cycling on whole heart function and booster the therapeutic potential of normalizing intracellular Ca(2+) cycling in patients with heart failure.
Authors:
Danny Guo; Gayatri Thiyam; Sreedhar Bodiga; Zamaneh Kassiri; Gavin Y Oudit
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-1-26
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  -     ISSN:  1095-8584     ISO Abbreviation:  -     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-1-31     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2010. Published by Elsevier Ltd.
Affiliation:
Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Canada; Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Canada.
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