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A Novel Method for Involving Women of Color at High Risk for Preterm Birth in Research Priority Setting
Published on: January 12, 2018
11β-HSD1 in Human Fetal Membranes as a Potential Therapeutic Target for Preterm Birth
Wangsheng Wang1,2, Zi-Jiang Chen1,2, Leslie Myatt3
1Center for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Abstract:
Human parturition is a complex process involving interactions between the myometrium and signals derived from the placenta, fetal membranes, and fetus. Signals originating from fetal membranes are crucial components that trigger parturition, which is clearly illustrated by the labor-initiating consequence of membrane rupture. It has been recognized for a long time that among fetal tissues in late gestation the fetal membranes possess the highest capacity for cortisol regeneration by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). However, the exact role of this unique feature remains a mystery. Accumulating evidence indicates that this extra-adrenal source of cortisol may serve as an upstream signal for critical events in human parturition, including enhanced prostaglandin and estrogen synthesis as well as extracellular matrix remodeling. This may explain why such high capacity for cortisol regeneration develops in human fetal membranes at late gestation. Therefore, inhibition of 11β-HSD1 may provide a potential therapeutic target for prevention of preterm birth. This review summarizes the current understanding of the functional role of cortisol regeneration by 11β-HSD1 in human fetal membranes.
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