Document Detail

Mechanisms underlying "functional" progesterone withdrawal at parturition.
MedLine Citation:
PMID:  15731298     Owner:  NLM     Status:  MEDLINE    
Progesterone is a major factor maintaining uterine quiescence throughout pregnancy. In most species, peripheral progesterone levels decline before initiation of labor, and treatments that inhibit progesterone synthesis or action cause termination of pregnancy and/or premature deliveries. These findings suggest that progesterone withdrawal is required for activation of myometrial contractions. However, in humans, circulating progesterone levels remain elevated until birth, which leads to the notion that a "functional" progesterone withdrawal occurs before parturition. The apparent loss of progesterone sensitivity at term could be a consequence of several different mechanisms including: (1) the catabolism of progesterone in the uterus into inactive compounds; (2) alterations in progesterone receptor (PR) isoform ratios; (3) changes in cofactor protein levels affecting PR transactivation; and (4) inflammation-induced trans-repression of PR by nuclear factor kappaB. All of these mechanisms are potentially capable of decreasing uterine progesterone responsiveness at term, thus enabling the expression of pathways that originally were blocked by progesterone in early pregnancy. However, the specific uterine genes whose transcription is directly controlled by PR, and thus affected by "functional" progesterone withdrawal, remain to be identified.
Amy G Brown; Rita S Leite; Jerome F Strauss
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Annals of the New York Academy of Sciences     Volume:  1034     ISSN:  0077-8923     ISO Abbreviation:  Ann. N. Y. Acad. Sci.     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2005-02-25     Completed Date:  2005-06-14     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  36-49     Citation Subset:  IM    
III 1354 Biomedical Research Building II/III, 421 Curie Boulevard, Philadelphia, PA 19104, USA.
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MeSH Terms
Parturition / physiology*
Progesterone / physiology*
Uterus / physiology*
Grant Support
Reg. No./Substance:

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