Progesterone receptor expression in human decidua and fetal membranes before and after contractions: possible mechanism for functional progesterone withdrawal

Goldman, Shlomit; Weiss, Amir; Almalah, Irit; Shalev, Eliezer

doi:10.1093/molehr/gah161

Cited by 70 publications

(77 citation statements)

References 36 publications

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“…There is also evidence that inflammation via NF-κB can reduce P 4 effectiveness and PGF 2α increases PR-A expression without affecting PR-B expression (69, 70). In addition, several studies reported that human labor is associated with reduced decidual expression of PR (71)(72)(73). Taken together, the evidence indicates that P 4 signaling in the context of myometrial contractility in human parturition requires further investigation.…”

Section: Figurementioning

confidence: 76%

Combinatory approaches prevent preterm birth profoundly exacerbated by gene-environment interactions

Cha¹,

Bartos²,

Egashira³

et al. 2013

J. Clin. Invest.

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There are currently more than 15 million preterm births each year. We propose that gene-environment interaction is a major contributor to preterm birth. To address this experimentally, we generated a mouse model with uterine deletion of Trp53, which exhibits approximately 50% incidence of spontaneous preterm birth due to premature decidual senescence with increased mTORC1 activity and COX2 signaling. Here we provide evidence that this predisposition provoked preterm birth in 100% of females exposed to a mild inflammatory insult with LPS, revealing the high significance of gene-environment interactions in preterm birth. More intriguingly, preterm birth was rescued in LPS-treated Trp53-deficient mice when they were treated with a combination of rapamycin (mTORC1 inhibitor) and progesterone (P 4 ), without adverse effects on maternal or fetal health. These results provide evidence for the cooperative contributions of two sites of action (decidua and ovary) toward preterm birth. Moreover, a similar signature of decidual senescence with increased mTORC1 and COX2 signaling was observed in women undergoing preterm birth. Collectively, our findings show that superimposition of inflammation on genetic predisposition results in high incidence of preterm birth and suggest that combined treatment with low doses of rapamycin and P 4 may help reduce the incidence of preterm birth in high-risk women.

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Section: Figurementioning

confidence: 76%

Combinatory approaches prevent preterm birth profoundly exacerbated by gene-environment interactions

Cha¹,

Bartos²,

Egashira³

et al. 2013

J. Clin. Invest.

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“…In biopsies of cervices from peripartum women, concentrations of progesterone receptor protein decreased at term to 25% of the level found in nonpregnant women [10]. Other recent findings suggest that PGF 2alpha promotes the expression of inhibitory progesterone receptor isoforms in myometrium from parturient women [11,12]. Thus, in rodents, as in primates, actions of PGF 2alpha may contribute to a reduced efficacy of progesterone and promote processes that enhance uterine contractility in preparation for parturition.…”

Section: Introductionmentioning

confidence: 92%

Parturition and Recruitment of Macrophages in Cervix of Mice Lacking the Prostaglandin F Receptor1

Yellon

Ebner

Sugimoto

2008

Biology of Reproduction

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“…Both PGRA and PGRB may activate different sets of genes, even within the same cell, revealing the enormous complexity of progesterone-dependent activation in the target cell (Graham & Clarke 2002, Alfaro et al 2012. This suggests that changes in the expression of PGR isoforms could regulate the biological activity of progesterone, resulting in functional hormone withdrawal at the ovarian level, under unchanged progesterone serum concentrations (Schams et al 2003, Amrozi et al 2004, Goldman et al 2005.…”

Section: R253mentioning

confidence: 99%

Molecular aspects of bovine cystic ovarian disease pathogenesis

Ortega¹,

Marelli²,

Rey³

et al. 2015

Reproduction

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Cystic ovarian disease (COD) is one of the main causes of reproductive failure in cattle and causes severe economic loss to the dairy farm industry because it increases both days open in the post partum period and replacement rates due to infertility. This disease is the consequence of the failure of a mature follicle to ovulate at the time of ovulation in the estrous cycle. This review examines the evidence for the role of altered steroid and gonadotropin signaling systems and the proliferation/apoptosis balance in the ovary with cystic structures. This evidence suggests that changes in the expression of ovarian molecular components associated with these cellular mechanisms could play a fundamental role in the pathogenesis of COD. The evidence also shows that gonadotropin receptor expression in bovine cystic follicles is altered, which suggests that changes in the signaling system of gonadotropins could play a fundamental role in the pathogenesis of conditions characterized by altered ovulation, such as COD. Ovaries from animals with COD exhibit a disrupted steroid receptor pattern with modifications in the expression of coregulatory proteins. These changes in the pathways of endocrine action would trigger the changes in proliferation and apoptosis underlying the aberrant persistence of follicular cysts. Free Spanish abstract: A Spanish translation of this abstract is freely available at

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Progesterone receptor expression in human decidua and fetal membranes before and after contractions: possible mechanism for functional progesterone withdrawal

Cited by 70 publications

References 36 publications

Combinatory approaches prevent preterm birth profoundly exacerbated by gene-environment interactions

Combinatory approaches prevent preterm birth profoundly exacerbated by gene-environment interactions

Parturition and Recruitment of Macrophages in Cervix of Mice Lacking the Prostaglandin F Receptor1

Molecular aspects of bovine cystic ovarian disease pathogenesis

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