Document Detail


Myosin from failing and non-failing human ventricles exhibit similar contractile properties.
MedLine Citation:
PMID:  12623303     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In non-failing human myocardium, V1 myosin comprises a small amount (<10%) of the total myosin content, whereas end-stage failing hearts contain nearly 100% V3 myosin. It has been suggested that this shift in V1 myosin isoform content may contribute to the contractile deficit in human myocardial failure. To test this hypothesis, myosin was isolated from human failing and non-failing ventricles, and non-failing atria. Performance was assessed in in vitro motility and isometric force assays. Consistent with prior reports, a small amount of V1 myosin was present in both non-failing (6.2 +/- 1.0%) and failing (3.5 +/- 1.4%) ventricular tissues. No difference in isometric force or unloaded shortening velocity was observed for failing and non-failing ventricular myosin irrespective of myosin isoform content. Atrial tissue expressing predominantly V1 myosin (66.7 +/- 4.1%) generated half the force but greater velocity compared with ventricular tissue, expressing predominantly V3 myosin. In additional experiments, rabbit cardiac myosin was used in a calcium regulated assay system to determine if V1 and V3 isoforms differentially affect thin filament activation. Half-maximal calcium activation was similar for the two cardiac isoforms. A 1:9 mixture of V1/V3 myosin, simulating isoform composition in non-failing human myocardium, was indistinguishable from 100% V3 myosin (simulating the failing state) with regard to velocity of shortening and average force. These data suggest that the myosin isoform shift reported in human myocardial failure does not significantly contribute to the contractile deficit of this disease.
Authors:
Teruo Noguchi; Phillip Camp; Shari L Alix; Joseph A Gorga; Kelly J Begin; Bruce J Leavitt; Frank P Ittleman; Norman R Alpert; Martin M LeWinter; Peter VanBuren
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  35     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2003 Jan 
Date Detail:
Created Date:  2003-03-07     Completed Date:  2003-09-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  91-7     Citation Subset:  IM    
Affiliation:
Cardiology Unit, Department of Medicine, College of Medicine, The University of Vermont, 121 HRSF Building, 149 Beaumont Avenue, Burlington, VT 05405, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Heart Failure / metabolism*
Humans
Myocardial Contraction / physiology*
Protein Isoforms / physiology
Rabbits
Ventricular Myosins / physiology*
Grant Support
ID/Acronym/Agency:
HL52087/HL/NHLBI NIH HHS; HL59408/HL/NHLBI NIH HHS; HL65586/HL/NHLBI NIH HHS; HL66157/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Protein Isoforms; EC 3.6.1.-/Ventricular Myosins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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