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Molecular Regulation of Parturition: A Myometrial Perspective
Nora E Renthal1, Koriand'r C Williams1, Alina P Montalbano1
1Department of Biochemistry, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-9038.
Cold Spring Harbor Perspectives in Medicine
|September 5, 2015
Summary
Progesterone and estradiol-17β regulate uterine contractility. In women, decreased progesterone receptor function, not levels, may drive labor by altering myometrial contractility.
Area of Science:
- Reproductive biology and endocrinology
- Molecular and cellular physiology
- Genetics and epigenetics
Background:
- Myometrial quiescence during pregnancy is maintained by progesterone (P4), which inhibits proinflammatory pathways and contractile gene expression.
- Estradiol-17β (E2) and estrogen receptor α (ERα) typically increase, with a P4 decline, to promote uterine contractility near term in most mammals.
- Unlike other mammals, women maintain elevated P4 and progesterone receptors (PR) throughout pregnancy and labor, suggesting a decline in PR function mediates contractility.
Purpose of the Study:
- To elucidate the molecular mechanisms governing myometrial quiescence and contractility.
- To investigate the regulatory roles of progesterone (P4) and estradiol-17β (E2) in pregnancy and labor.
- To explore the involvement of microRNAs in mediating myometrial responses to hormonal changes.
Main Methods:
- Review and integration of existing literature on hormonal regulation of the myometrium.
- Analysis of molecular pathways involved in progesterone and estrogen signaling.
- Consideration of microRNA involvement in myometrial gene expression and function.
Main Results:
- Progesterone (P4) is crucial for maintaining uterine quiescence by suppressing inflammatory responses and contractile gene expression.
- Estradiol-17β (E2) and estrogen receptor α (ERα) activity influence uterine contractility, typically alongside a P4 decline in most species.
- In humans, elevated P4 and PR levels persist into labor, indicating that a functional decline in PR, rather than absolute levels, is key to initiating labor.
Conclusions:
- The transition from myometrial quiescence to labor involves complex hormonal interplay, primarily regulated by progesterone (P4) and estradiol-17β (E2).
- A functional decrease in progesterone receptor (PR) activity, despite sustained PR levels, is a critical factor in human labor initiation.
- MicroRNAs play an integrative role in modulating the molecular mechanisms underlying myometrial contractility and quiescence throughout pregnancy.
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