Linked Life Data

15013796

Source:http://linkedlifedata.com/resource/pubmed/id/15013796

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-3-11
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0012-1606
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
267
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
309-19
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Fas ligand gene transfer to the embryonic heart induces programmed cell death and outflow tract defects.
pubmed:affiliation
Department of Pediatrics (Cardiology), Case Western Reserve School of Medicine, Cleveland, OH 44106, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't