Document Detail


Suppression of extravillous trophoblast vascular endothelial growth factor expression and uterine spiral artery invasion by estrogen during early baboon pregnancy.
MedLine Citation:
PMID:  18566115     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have shown that advancing the increase in maternal serum estrogen levels from the second to the first third of baboon pregnancy suppressed extravillous cytotrophoblast (EVT) spiral artery invasion. Because vascular endothelial growth factor (VEGF) promotes EVT invasion, the present study determined whether EVT VEGF expression is altered by prematurely elevating estrogen in early pregnancy. Placental basal plate was obtained on d 60 of gestation (term is 184 d) from baboons treated daily on d 25-59 with estradiol (0.35 mg/d sc), which increased maternal peripheral serum estradiol levels 3-fold above normal. Overall percentage of uterine arteries (25 to more than 100 microm in diameter) invaded by EVT assessed by image analysis in untreated baboons (29.11+/-5.78%) was decreased 4.5-fold (P<0.001) by prematurely elevating estrogen (6.55+/-1.83%). VEGF mRNA levels in EVT isolated by laser capture microdissection from the anchoring villi of untreated baboons (6.77+/-2.20) were decreased approximately 5-fold (P<0.05, ANOVA) by estradiol (1.37+/-0.29). Uterine vein serum levels of the truncated soluble fms-like receptor, which controls VEGF bioavailability, in untreated baboons (403+/-37 pg/ml) were increased 3-fold (P<0.01) by estrogen treatment (1127+/-197 pg/ml). Thus, placental EVT expression of VEGF mRNA was decreased and serum soluble truncated fms-like receptor levels increased in baboons in which EVT invasion of the uterine spiral arteries was suppressed by advancing the rise in estrogen from the second to the first third of pregnancy. We suggest that VEGF mediates the decline in EVT vessel invasion induced by estrogen in early primate pregnancy.
Authors:
Thomas W Bonagura; Gerald J Pepe; Allen C Enders; Eugene D Albrecht
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2008-06-19
Journal Detail:
Title:  Endocrinology     Volume:  149     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-09-23     Completed Date:  2008-11-04     Revised Date:  2014-10-17    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5078-87     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Weight
Estrogens / blood*,  pharmacology
Female
Gestational Age
Immunohistochemistry
Organ Size
Papio anubis
Pregnancy
Pregnancy, Animal / physiology*
RNA, Messenger / metabolism
Solubility
Trophoblasts / physiology*
Uterus / blood supply*,  cytology
Vascular Endothelial Growth Factor A / genetics*
Vascular Endothelial Growth Factor Receptor-1 / blood,  genetics*
Grant Support
ID/Acronym/Agency:
R01 HD013294/HD/NICHD NIH HHS; R01 HD013294-28/HD/NICHD NIH HHS; R01 HD13294/HD/NICHD NIH HHS; U54 HD036207/HD/NICHD NIH HHS; U54 HD36207/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Estrogens; 0/RNA, Messenger; 0/Vascular Endothelial Growth Factor A; EC 2.7.10.1/Vascular Endothelial Growth Factor Receptor-1
Comments/Corrections

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


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