Document Detail


2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibition of coronary vasculogenesis is mediated, in part, by reduced responsiveness to endogenous angiogenic stimuli, including vascular endothelial growth factor A (VEGF-A).
MedLine Citation:
PMID:  15880788     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure prior to chick embryo incubation (GD 0) induces dilated cardiomyopathy, and reduces myocardial hypoxia, vascular endothelial growth factor A (VEGF-A) expression, and coronary vascularization. We investigated whether reduced coronary vascularization 1) occurs in the absence of changes in cardiac morphology and 2) is associated with altered secretion of VEGF-A and/or an antivasculogenic factor. METHODS: Chicken eggs were treated with control (corn oil) or TCDD (0.075-0.3 pmol of TCDD/gm) on GD 5. In vivo cardiac morphology and artery number were determined on GD 10, while in vitro vascular outgrowth and VEGF-A secretion were determined from cardiac explants on GD 6. Effects of recombinant VEGF-A (rcVEGF-A), soluble flt-1 (sFlt-1) receptor plus rcVEGF-A, and control conditioned media were assessed in TCDD explants, while effects of TCDD-conditioned media was assessed in control explants. RESULTS: TCDD reduced coronary artery number in vivo by 53 +/- 8% and induced a dose-related reduction in tube outgrowth in vitro, but had no effect on cardiac morphology. All TCDD doses reduced explant VEGF-A secretion equally (43 +/- 3%), compared to control. sFlt-1 blocked outgrowth in control cultures and blocked rcVEGF-A-mediated rescue of outgrowth in TCDD explants. Control conditioned media partially rescued outgrowth from TCDD explants, while conditioned media from TCDD explants had no effect on controls. CONCLUSIONS: TCDD inhibition of coronary vascularization can occur in the absence of changes in cardiac morphology and is associated with reduced VEGF-A secretion but not an antivasculogenic factor. Since control media only partly rescues TCDD's inhibitory effect, we suggest that TCDD-exposed endothelial cells are less responsive to vasculogenic stimuli.
Authors:
Irena D Ivnitski-Steele; Megan Friggens; Miquella Chavez; Mary K Walker
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Birth defects research. Part A, Clinical and molecular teratology     Volume:  73     ISSN:  1542-0752     ISO Abbreviation:  Birth Defects Res. Part A Clin. Mol. Teratol.     Publication Date:  2005 Jun 
Date Detail:
Created Date:  2005-06-13     Completed Date:  2005-10-04     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  101155107     Medline TA:  Birth Defects Res A Clin Mol Teratol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  440-6     Citation Subset:  IM    
Copyright Information:
(c) 2005 Wiley-Liss, Inc.
Affiliation:
College of Pharmacy, University of New Mexico, Albuquerque, NM 87131, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiogenesis Inducing Agents / pharmacology*
Animals
Chick Embryo
Coronary Vessels / drug effects*,  embryology
Fibroblast Growth Factor 2 / pharmacology
Tetrachlorodibenzodioxin / toxicity*
Vascular Endothelial Growth Factor A / pharmacology
Grant Support
ID/Acronym/Agency:
P30 ES 012072/ES/NIEHS NIH HHS; R01 ES 09804/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Angiogenesis Inducing Agents; 0/Vascular Endothelial Growth Factor A; 103107-01-3/Fibroblast Growth Factor 2; 1746-01-6/Tetrachlorodibenzodioxin

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


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