Linked Life Data

10653528

Source:http://linkedlifedata.com/resource/pubmed/id/10653528

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-2-15
pubmed:abstractText
Previous epidemiological studies with humans and laboratory studies with chickens and rats linked trichloroethylene (TCE) exposure to cardiac defects. Although the cardiac defects in humans and laboratory animals produced by TCE are diverse, a majority of them involves valvular and septal structures. Progenitors of the valves and septa are formed by an epithelial-mesenchymal cell transformation of endothelial cells in the atrioventricular (AV) canal and outflow tract areas of the heart. Based on these studies, we hypothesized that TCE might cause cardiac valve and septa defects by specifically perturbing epithelial-mesenchymal cell transformation. We tested this hypothesis using an in vitro chick-AV canal culture model. This study shows that TCE affected several elements of epithelial-mesenchymal cell transformation. In particular, TCE blocked the endothelial cell-cell separation process that is associated with endothelial activation. Moreover, TCE inhibited mesenchymal cell formation throughout the concentration range tested (50-250 ppm). In contrast, TCE had no effect on the cell migration rate of the fully formed mesenchymal cells. Finally, the expression of 3 proteins (selected as molecular markers of epithelial-mesenchymal cell transformation) was analyzed in untreated and TCE-treated cultures. TCE inhibited the expression of the transcription factor Mox-1 and extracellular matrix (ECM) protein fibrillin 2. In contrast, TCE had no effect on the expression of alpha-smooth muscle actin. These data suggest that TCE may cause cardiac valvular and septal malformations by inhibiting endothelial separation and early events of mesenchymal cell formation in the heart.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1096-6080
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
109-17
pubmed:dateRevised
2010-9-17
pubmed:meshHeading
pubmed-meshheading:10653528-Actins, pubmed-meshheading:10653528-Alcohol Oxidoreductases, pubmed-meshheading:10653528-Animals, pubmed-meshheading:10653528-Cell Count, pubmed-meshheading:10653528-Cell Differentiation, pubmed-meshheading:10653528-Cell Movement, pubmed-meshheading:10653528-Cells, Cultured, pubmed-meshheading:10653528-Chick Embryo, pubmed-meshheading:10653528-Dose-Response Relationship, Drug, pubmed-meshheading:10653528-Endocardial Cushion Defects, pubmed-meshheading:10653528-Endothelium, pubmed-meshheading:10653528-Epithelial Cells, pubmed-meshheading:10653528-Fluorescent Antibody Technique, Indirect, pubmed-meshheading:10653528-Heart Valves, pubmed-meshheading:10653528-Mesoderm, pubmed-meshheading:10653528-Microfilament Proteins, pubmed-meshheading:10653528-Trichloroethylene
pubmed:year
2000
pubmed:articleTitle
Trichloroethylene inhibits development of embryonic heart valve precursors in vitro.
pubmed:affiliation
Department of Cell Biology and Anatomy, University of Arizona, Tucson 85724, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't