The steroid hormone progesterone (P4), acting via the nuclear P4 receptors (PRs) in uterine cells, is essential for the establishment and maintenance of pregnancy. P4/PR signaling maintains pregnancy by promoting uterine quiescence and blocking the contractions of labor. Withdrawal of the P4/PR block to labor induces parturition. The success of pregnancy requires the timely birth of a mature neonate to a healthy mother, and to this end, the mechanism by which the P4/PR block is withdrawn, and how that process is physiologically controlled is critical. This review examines current understanding of cell and molecular biology of P4/PR withdrawal in the control of parturition.
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Progesterone withdrawal and parturition.
J Steroid Biochem Mol Biol
November 2022
William H Weir MD Professor of Reproductive Biology, Department of Reproductive Biology Case, Western Reserve University, USA; Department of Obstetrics and Gynecology, University Hospitals of Cleveland, 11100 Euclid Ave, Cleveland, OH 44106, USA. Electronic address:
The steroid hormone progesterone (P4), acting via the nuclear P4 receptors (PRs) in uterine cells, is essential for the establishment and maintenance of pregnancy. P4/PR signaling maintains pregnancy by promoting uterine quiescence and blocking the contractions of labor. Withdrawal of the P4/PR block to labor induces parturition.
View Article and Find Full Text PDFProgestin therapy to prevent preterm birth: History and effectiveness of current strategies and development of novel approaches.
Placenta
April 2019
Department of Biochemistry, Case Western Reserve University, Cleveland, OH, USA.
In the 1930s the "progestin" hormone produced by the corpus luteum was isolated and found to be a Δ-keto-steroid. It was aptly named progesterone (P4) and in the following 30 years the capacity of P4 and derivatives to prevent preterm birth (PTB) was examined. Outcomes of multiple small studies suggested that progestin prophylaxis beginning at mid-gestation decreases the risk for PTB.
View Article and Find Full Text PDFExpression and function of myometrial PSF suggest a role in progesterone withdrawal and the initiation of labor.
Mol Endocrinol
August 2012
Vancouver Prostate Center, Department of Urologic Sciences, University of British Columbia, Vancouver Canada.
Article Synopsis
- Progesterone (P4) is crucial for maintaining pregnancy by inhibiting uterine contractions and the expression of contraction-related proteins like connexin 43 (Cx43).
- For labor to begin, P4 levels must decrease or its effects need to be blocked, allowing the expression of contraction-associated proteins and the initiation of labor.
- The study identifies that the interaction between the ligand-bound progesterone receptor (PR) and the Cx43 gene promoter involves specific transcription factors and coregulators, highlighting the role of polypyrimidine tract binding protein-associated splicing factor (PSF) in regulating progesterone signaling and the transition to labor.
Progesterone reverses the mesenchymal phenotypes of basal phenotype breast cancer cells via a membrane progesterone receptor mediated pathway.
Breast Cancer Res
November 2010
Atlanta Research & Educational Foundation, Atlanta VA Medical Center, 1670 Clairmont Road, Decatur, GA 30033, USA.
Introduction: Basal phenotype breast cancers (BPBC) are often associated with apparent epithelial to mesenchymal transition (EMT). The role of progesterone (P4) in regulating EMT of BPBC has not been reported.
Methods: The EMT relevant biology was investigated in vitro using human BPBC cell models (MDA-MB468 and MDA-MB231) with P4, PR agonist (RU486), and PR antagonist (R5020) treatments.
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