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Mechanisms Underlying "Functional" Progesterone Withdrawal at Parturition
AMY G. BROWN,
RITA S. LEITE AND
JEROME F. STRAUSS, III
Center for Research on Reproduction and Women's Health, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
Address for correspondence: Jerome F. Strauss, III M.D., Ph.D., 1354 Biomedical Research Building II/III, 421 Curie Boulevard, Philadelphia, PA 19104. Voice: (215) 898-0147; fax: (215)-573-5408. jfs3{at}mail.med.upenn.edu
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  B. 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.
Key Words: progesterone receptor • parturition • "functional" progesterone withdrawal • uterus • labor
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