Document Detail


In vivo studies on nonmuscle myosin II expression and function in heart development.
MedLine Citation:
PMID:  22201759     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nonmuscle myosin II-B (NM II-B) plays an important role in cardiac development and function. Genetic ablation of NM II-B in mice results in both cellular and structural defects involving cardiac myocytes. These abnormalities include a ventricular septal defect, double outlet of the right ventricle, myocyte hypertrophy and premature onset of myocyte binucleation due to abnormalities in cytokinesis. The mice die by embryonic day (E) 14.5 due to defects in heart development. Conditional ablation of NM II-B in cardiac myocytes after E11.5 allows study of NM II-B function in adult myocytes. BaMHC/BaMHC mice are born with enlarged cardiac myocytes, some of which are multinucleated. Between 6-10 months of age they develop a cardiomyopathy. Many of these mice develop a marked widening of the intercalated discs. The loss of NM II-B from the intercalated discs primarily affects the adhesion junctions rather than the gap junctions and desmosomes. Interestingly, the loss of NM II-B results in a decrease in the actin binding protein mXin which also has been shown to cause disruption of the intercalated disc in addition to cardiac arrhythmias (Gustafson-Wagner et al. Am J Physiol Heart Circ Physiol. 2007, 293:H2680-92). Finally we review the evidence showing that ablation of NM II-C (which also localizes to the intercalated disc) in mouse hearts deficient in NM II-B expression results in destabilization of N-cadherin and beta-catenin in the intercalated disc.
Authors:
Xuefei Ma; Robert S Adelstein
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Publication Detail:
Type:  Journal Article; Review     Date:  2012-01-01
Journal Detail:
Title:  Frontiers in bioscience (Landmark edition)     Volume:  17     ISSN:  1093-4715     ISO Abbreviation:  Front Biosci (Landmark Ed)     Publication Date:  2012  
Date Detail:
Created Date:  2011-12-28     Completed Date:  2012-05-24     Revised Date:  2013-07-29    
Medline Journal Info:
Nlm Unique ID:  101612996     Medline TA:  Front Biosci (Landmark Ed)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  545-55     Citation Subset:  IM    
Affiliation:
Laboratory of Molecular Cardiology, NHLBI, National Institutes of Health, Bethesda, MD 20892, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Fetal Heart / embryology*,  physiology*
Gene Expression Regulation, Developmental
Mice
Models, Molecular
Myocardium / metabolism
Nonmuscle Myosin Type IIB / chemistry,  genetics*,  physiology*
Protein Isoforms / chemistry,  genetics,  physiology
Grant Support
ID/Acronym/Agency:
Z01 HL004228-13/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Protein Isoforms; EC 3.6.1.-/Nonmuscle Myosin Type IIB
Comments/Corrections

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