Molecular Regulation of Parturition: A Myometrial Perspective

Cold Spring Harbor Perspectives in Medicine
Nora E RenthalCarole R Mendelson

Abstract

The molecular mechanisms that maintain quiescence of the myometrium throughout most of pregnancy and promote its transformation to a highly coordinated contractile unit culminating in labor are complex and intertwined. During pregnancy, progesterone (P4) produced by the placenta and/or ovary serves a dominant role in maintaining myometrial quiescence by blocking proinflammatory response pathways and expression of so-called "contractile" genes. In the majority of placental mammals, increased uterine contractility near term is heralded by an increase in circulating estradiol-17β (E2) and/or increased estrogen receptor α (ERα) activity and a sharp decline in circulating P4 levels. However, in women, circulating levels of P4 and progesterone receptors (PR) in myometrium remain elevated throughout pregnancy and into labor. This has led to the concept that increased uterine contractility leading to term and preterm labor is mediated, in part, by a decline in PR function. The biochemical mechanisms for this decrease in PR function are also multifaceted and interwoven. In this paper, we focus on the molecular mechanisms that mediate myometrial quiescence and contractility and their regulation by the two central hormones of pregnancy, P...Continue Reading

Citations

Jun 16, 2016·Reproductive Biology and Endocrinology : RB&E·Judit Hajagos-TóthRóbert Gáspár
Feb 27, 2017·Journal of Biochemical and Molecular Toxicology·Pablo Dominguez-LopezFabian Arechavaleta-Velasco
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Jul 28, 2016·The Journal of Clinical Endocrinology and Metabolism·Lu GaoCarole R Mendelson
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Jun 12, 2021·Journal of Cellular and Molecular Medicine·Lubna NadeemStephen J Lye
Jul 6, 2021·Frontiers in Endocrinology·Melissa L KozakiewiczAllyn C Howlett

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