Document Detail


Cortisol blockade of progesterone: a possible molecular mechanism involved in the initiation of human labor.
MedLine Citation:
PMID:  8616715     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In most mammals, labor is heralded by progesterone withdrawal, which is believed to be related to the activation of multiple pathways leading to parturition. In humans, despite no decrease in placental progesterone production, activation of similar pathways preceding labor suggests the presence of an endogenous antiprogestin, which we reasoned might be cortisol, whose secretion from the fetal adrenal rises markedly at the end of human gestation. We report that in primary cultures of human placenta, cortisol is able to compete with the action of progesterone in the regulation of the corticotropin-releasing hormone (CRH) gene. CRH is a peptide highly expressed in human placenta at the end of gestation, which has been suggested to be involved in regulating the timing of parturition. These findings provide a model for functional progesterone withdrawal at the end of human pregnancy, which may be involved in the initiation of labor.
Authors:
K Karalis; G Goodwin; J A Majzoub
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Nature medicine     Volume:  2     ISSN:  1078-8956     ISO Abbreviation:  Nat. Med.     Publication Date:  1996 May 
Date Detail:
Created Date:  1996-06-13     Completed Date:  1996-06-13     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9502015     Medline TA:  Nat Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  556-60     Citation Subset:  IM    
Affiliation:
Division of Endocrinology, Children's Hospital, Boston, Massachusetts 02115, USA.
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MeSH Terms
Descriptor/Qualifier:
Cells, Cultured
Corticotropin-Releasing Hormone / biosynthesis*
Female
Fetus / physiology
Humans
Hydrocortisone / pharmacology*
Labor Onset / physiology*
Models, Biological
Pregnancy
Progesterone / antagonists & inhibitors*
Receptors, Glucocorticoid / analysis
Receptors, Progesterone / analysis
Trophoblasts / cytology,  physiology*
Grant Support
ID/Acronym/Agency:
2MO1 RR 02172/RR/NCRR NIH HHS; R01 HD 24704-05/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Glucocorticoid; 0/Receptors, Progesterone; 50-23-7/Hydrocortisone; 57-83-0/Progesterone; 9015-71-8/Corticotropin-Releasing Hormone

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


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