Document Detail


Fas ligand gene transfer to the embryonic heart induces programmed cell death and outflow tract defects.
MedLine Citation:
PMID:  15013796     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The remodeling of the embryonic avian cardiac outflow tract (OFT) involves the removal of cardiomyocytes by programmed cell death (PCD). In contrast, the prevalence of PCD is low in the atrial or ventricular myocytes during this period of development. To determine if this selective PCD is due to the unique ability of the OFT cardiomyocytes to execute PCD, we transduced the embryonic chicken heart in ovo with recombinant adenovirus expressing a death (FasL) ligand. This resulted in programmed cell death in atrial, ventricular, and OFT cardiomyocytes as evidenced by chromosomal fragmentation, accumulation of lysosomes, and Caspase enzymatic activity. Consistent with the widespread induction of PCD, transcripts for the Fas receptor were detected in all chambers of the heart throughout development. The precocious and widespread activation of PCD in the OFT myocardium resulted in a marked dimunition of the subpulmonic myocardial infundibulum, and transposition of the aorta side-by-side with the pulmonary artery and connecting to the right ventricle. Defects in other cardiac structures are also described. We conclude that the regulated removal of OFT cardiomyocytes by PCD is required for the great vessels to make their proper connections with the ventricles in the transition to a dual circulation. The malalignment of the great vessels described in this animal model are similar to those described in congenital human conotruncal heart defects, suggesting that PCD-dependent remodeling of the OFT myocardium could be a target of genetic mutations or teratogens that cause human conotruncal heart defects.
Authors:
Denver Sallee; Yaling Qiu; Jun Liu; Michiko Watanabe; Steven A Fisher
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Developmental biology     Volume:  267     ISSN:  0012-1606     ISO Abbreviation:  Dev. Biol.     Publication Date:  2004 Mar 
Date Detail:
Created Date:  2004-03-11     Completed Date:  2004-05-04     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0372762     Medline TA:  Dev Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  309-19     Citation Subset:  IM    
Affiliation:
Department of Pediatrics (Cardiology), Case Western Reserve School of Medicine, Cleveland, OH 44106, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Caspases / metabolism
Chick Embryo
DNA Primers
Fas Ligand Protein
Gene Expression*
Heart / anatomy & histology,  embryology*
Histological Techniques
In Situ Hybridization
Membrane Glycoproteins / metabolism*
Morphogenesis
Myocardium / cytology*,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Transduction, Genetic
Grant Support
ID/Acronym/Agency:
HL-03275/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/DNA Primers; 0/FASLG protein, human; 0/Fas Ligand Protein; 0/Membrane Glycoproteins; EC 3.4.22.-/Caspases

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


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