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Human atrial myosin light chain 1 expression attenuates heart failure

Item Type:Article
Title:Human atrial myosin light chain 1 expression attenuates heart failure
Creators Name:Abdelaziz, A.I. and Pagel, I. and Schlegel, W.P. and Kott, M. and Monti, J. and Haase, H. and Morano, I.
Abstract:Most patients with hypertrophie cardiomyopathy and congenital heart diseases express the atrial essential myosin light chains (ALC-1) in their ventricles, replacing the ventricular essential light chains (VLC-1). VLC-1/ALC-1 isoform shift is correlated with increases in cardiac contractile parameters of a transgenic rat model overexpressing hALC-1 in the heart (TGR/hALC-1) compared to normal WKY rats. To investigate, whether the benefical effects of the hALC-1 on cardiac contractility could attenuate contractile failure of the overloaded heart, aortocaval shunt operations of 9-10 weeks old WKY and TGR/hALC-1 were performed. 5 weeks later, both animals groups were sacrificed for analysis of cardiac contraction and transgene expression. Control animals were operated but remained normal body and heart weights. The whole heart contractility parameters were evaluated using the Langendorff heart preparation. Shunt-operated TGR/hALC-1 and WKY rats developed comparable levels of cardiac hypertrophy which was associated with significant reduction of contractile parameters of the Langendorff hearts. However, the decline of cardiac contractility-was- less pronounced in shunt-operated TGR/hALC-1 compared to shunt-operated WKY. In fact, developed left ventricular pressure as well as maximal velocity of pressure development and relaxation were significantly higher in shunt-operated TGR/hALC-1 as compared to shunt-operated WKY. Expression of hALC-1 was 17μg/mg whole SDS-protein in control (sham-operated) controls and declined significantly to 14 μg/mg whole SDS-protein in hypertrophied TGR/hALC-1. These results demonstrate that the expression of hALC-1 could have a beneficial effect on the overloaded hypertrophied heart.
Keywords:Animal Disease Models, Cardiomyopathies, Gene Expression, Genetically Modified Animals, Heart Atria, Myocardial Contraction, Myosin Light Chains, Perfusion, Animals, Rats
Source:Advances in Experimental Medicine and Biology
Page Range:283-292
Date:1 January 2005
Official Publication:https://doi.org/10.1007/0-387-24990-7_21
PubMed:View item in PubMed

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