Document Detail

Angiotensin II type 1 receptor has impact on murine placentation.
MedLine Citation:
PMID:  18722658     Owner:  NLM     Status:  MEDLINE    
Impaired placentation is a key step in the pathogenesis of important pregnancy disorders such as preeclampsia and fetal growth restriction. A role of angiotensin II in placental development can be assumed from the expression of angiotensin receptors on trophoblast from the earliest stages of pregnancy. To understand the role of angiotensin II type 1 (AT1) receptors in placental development, we investigated placentae of AT1a-deficient mice early in pregnancy (day 13 postconception). The number of alive newborns was significantly reduced in AT1a-deficient mice caused by placental malformations in 30% of all utero-placental units. Importantly, no embryonic structure was observable within the uterine segments harboring the malformed placentae. Immunohistochemistry with an antibody against murine betahCG-equivalent stained homogeneously in almost all cells in the altered placentae indicating still an endocrine-active trophoblast. However, the typical structure of the murine wild-type placenta in spongiotrophoblast, giant cells, and labyrinth was abolished in malformed placental tissue deficient in the AT1a receptor. Recent epidemiological studies revealed the detrimental effect of an AT1 blockade for fetal outcome due to renal malformations and a reduced birth weight. For the latter, our findings provide an early mechanistic explanation. The lack in AT1 stimulation causes an impaired trophoblast maturation leading to impaired placental function.
T Walther; A Jank; S Heringer-Walther; L-C Horn; H Stepan
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Publication Detail:
Type:  Journal Article     Date:  2008-08-22
Journal Detail:
Title:  Placenta     Volume:  29     ISSN:  0143-4004     ISO Abbreviation:  Placenta     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-09-15     Completed Date:  2008-11-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  England    
Other Details:
Languages:  eng     Pagination:  905-9     Citation Subset:  IM    
Department of Cardiology and Pneumology, Charité, Campus Benjamin Franklin, Hindenburgdamm 30, Berlin, Germany.
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MeSH Terms
Adaptor Proteins, Signal Transducing / deficiency,  physiology*
Litter Size
Mice, Knockout
Mice, Transgenic
Placenta / growth & development,  pathology,  physiology*
Receptor, Angiotensin, Type 1 / physiology*
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Agtrap protein, mouse; 0/Receptor, Angiotensin, Type 1

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