Document Detail


Myocardial deletion of Smad4 using a novel α skeletal muscle actin Cre recombinase transgenic mouse causes misalignment of the cardiac outflow tract.
MedLine Citation:
PMID:  20877696     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
SMAD4 acts as the converging point for TGFβ and BMP signaling in heart development. Here, we investigated the role of SMAD4 in heart development using a novel α skeletal muscle actin Cre recombinase (MuCre) transgenic mouse strain. Lineage tracing using MuCre/ROSA26(LacZ) reporter mice indicated strong Cre-recombinase expression in developing and adult heart and skeletal muscles. In heart development, significant MuCre expression was noted at E11.5 in the atrial, ventricular, outflow tract and atrioventricular canal myocardium, but not in the endocardial cushions. MuCre-driven conditional deletion of Smad4 in mice caused double outlet right ventricle (DORV), ventricular septal defect (VSD), impaired trabeculation and thinning of ventricular myocardium, and mid-gestational embryonic lethality. In conclusion, MuCre mice effectively delete genes in both heart and skeletal muscles, thus enabling the discovery that myocardial Smad4 deletion causes misalignment of the outflow tract and DORV.
Authors:
Mohamad Azhar; Pei-Yu Wang; Tony Frugier; Kyoko Koishi; Chuxia Deng; Peter G Noakes; Ian S McLennan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-09-20
Journal Detail:
Title:  International journal of biological sciences     Volume:  6     ISSN:  1449-2288     ISO Abbreviation:  Int. J. Biol. Sci.     Publication Date:  2010  
Date Detail:
Created Date:  2010-09-29     Completed Date:  2011-01-19     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  101235568     Medline TA:  Int J Biol Sci     Country:  Australia    
Other Details:
Languages:  eng     Pagination:  546-55     Citation Subset:  IM    
Affiliation:
BIO5 Institute, and Department of Cell Biology and Anatomy, University of Arizona, Tucson, AZ 85724, USA. azharm@email.arizona.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Heart / embryology*
Humans
Integrases / genetics,  metabolism*
Mice
Mice, Transgenic
Morphogenesis / genetics,  physiology
Muscle, Skeletal / metabolism*
Myocardium / metabolism*
Smad4 Protein / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
R01 HL92508/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Smad4 Protein; EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases
Comments/Corrections

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