Document Detail


Developmental remodeling and shortening of the cardiac outflow tract involves myocyte programmed cell death.
MedLine Citation:
PMID:  9729489     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The embryonic outflow tract is a simple tubular structure that connects the single primitive ventricle with the aortic sac and aortic arch arteries. This structure undergoes a complex sequence of morphogenetic processes to become the portion of the heart that aligns the right and left ventricles with the pulmonary artery and aorta. Abnormalities of the outflow tract are involved in many clinically significant congenital cardiac defects; however, the cellular and molecular processes governing the development of this important structure are incompletely understood. Histologic and tissue-tagging studies indicate that the outflow tract tissues compact and are incorporated predominantly into a region of the right ventricle. The hypothesis tested in the current study was that cell death or apoptosis in the muscular portion of the outflow tract is an important cellular mechanism for outflow tract shortening. The tubular outflow tract myocardium was specifically marked by infecting myocytes of the chicken embryo heart with a recombinant replication-defective adenovirus expressing beta-galactosidase (beta-gal) under the control of the cytomegalovirus promoter. Histochemical detection of the beta -gal-labeled outflow tract myocytes revealed that the tubular structure shortened to become a compact ring at the level of the pulmonic infundibulum over several days of development (stages 25-32, embryonic days 4-8). The appearance of apoptotic cardiomyocytes was correlated with OFT shortening by two histologic assays, TUNEL labeling of DNA fragments and AnnexinV binding. The rise and fall in the number of apoptotic myocytes detected by histologic analyses paralleled the change in activity levels of Caspase-3, a protease in the apoptotic cascade, measured in outflow tract homogenates. These results suggest that the elimination of myocytes by programmed cell death is one mechanism by which the outflow tract myocardium remodels to form the proper connection between the ventricular chambers and the appropriate arterial trunks.
Authors:
M Watanabe; A Choudhry; M Berlan; A Singal; E Siwik; S Mohr; S A Fisher
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  125     ISSN:  0950-1991     ISO Abbreviation:  Development     Publication Date:  1998 Oct 
Date Detail:
Created Date:  1998-11-25     Completed Date:  1998-11-25     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  3809-20     Citation Subset:  IM    
Affiliation:
Division of Pediatric Cardiology, Department of Pediatrics, Rainbow Babies and Childrens Hospital, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. mxw13@po.cwru.edu
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MeSH Terms
Descriptor/Qualifier:
Adenoviridae / genetics
Animals
Annexin A5 / metabolism
Apoptosis* / genetics,  physiology
Caspase 3
Caspases / metabolism
Chick Embryo
Gene Expression Regulation, Developmental
Genes, Reporter
Genetic Vectors
Heart / embryology*
In Situ Nick-End Labeling
Myocardium / cytology*,  metabolism
Promoter Regions, Genetic
beta-Galactosidase / genetics
Grant Support
ID/Acronym/Agency:
HL38172/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Annexin A5; EC 3.2.1.23/beta-Galactosidase; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases

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


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