Document Detail


{beta}-Myosin Heavy Chain Is Induced by Pressure Overload in a Minor Subpopulation of Smaller Mouse Cardiac Myocytes.
MedLine Citation:
PMID:  21778428     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Rationale: Induction of the fetal hypertrophic marker gene β-myosin heavy chain (β-MyHC) is a signature feature of pressure overload hypertrophy in rodents. β-MyHC is assumed present in all or most enlarged myocytes. Objective: To quantify the number and size of myocytes expressing endogenous β-MyHC by a flow cytometry approach. Methods and Results: Myocytes were isolated from the left ventricle of male C57Bl/6J mice after transverse aortic constriction (TAC), and the fraction of cells expressing endogenous β-MyHC was quantified by flow cytometry on 10 000 to 20 000 myocytes with use of a validated β-MyHC antibody. Side scatter by flow cytometry in the same cells was validated as an index of myocyte size. β-MyHC(+) myocytes constituted 3±1% of myocytes in control hearts (n=12), increasing to 25±10% at 3 days to 6 weeks after TAC (n=24, P<0.01). β-MyHC(+) myocytes did not enlarge with TAC and were smaller at all times than myocytes without β-MyHC (≈70% as large, P<0.001). β-MyHC(+) myocytes arose by addition of β-MyHC to α-MyHC and had more total MyHC after TAC than did the hypertrophied myocytes that had α-MyHC only. Myocytes positive for β-MyHC were found in discrete regions of the left ventricle in 3 patterns: perivascular, in areas with fibrosis, and in apparently normal myocardium. Conclusions: β-MyHC protein is induced by pressure overload in a minor subpopulation of smaller cardiac myocytes. The hypertrophied myocytes after TAC have α-MyHC only. These data challenge the current paradigm of the fetal hypertrophic gene program and identify a new subpopulation of smaller working ventricular myocytes with more myosin.
Authors:
Javier E López; Bat-Erdene Myagmar; Philip M Swigart; Megan D Montgomery; Stephen Haynam; Marty Bigos; Manoj C Rodrigo; Paul C Simpson
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-7-21
Journal Detail:
Title:  Circulation research     Volume:  -     ISSN:  1524-4571     ISO Abbreviation:  -     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-7-22     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
VA Medical Center.
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