Abstract
Prokineticin 1 (PROK1) is a key regulator of embryo implantation and placentation, and its dysregulation is associated with pregnancy complications, such as pre‐eclampsia and foetal growth restriction. We have previously shown that insulin strongly enhances the expression of PROK1 in human decidualizing stromal cells. Here, we demonstrate that dihydrotestosterone (DHT), but not testosterone, potentiates insulin to up‐regulate PROK1 in these cells. However, the androgens alone do not influence the expression of PROK1. Our findings suggest that insulin and androgens both are involved in the regulation of PROK1 that could have implications for normal and pathological pregnancies.
Highlights
Trophoblast invasion of decidua and maternal spiral arteries is the key process in the establishment of feto-maternal circulation in early pregnancy
Prokineticin 1 (PROK1) promotes the proliferation of cytotrophoblasts at the expense of their differentiation and by this contributes to the formation and maintenance of trophoblastic plugs in the maternal spiral arteries that protects the developing foetus and placenta from highly oxygenated maternal blood
Dysregulation of PROK1 has been associated with placenta-related pregnancy complications, such as pre-eclampsia and intrauterine growth restriction.[2,3,4]
Summary
Trophoblast invasion of decidua and maternal spiral arteries is the key process in the establishment of feto-maternal circulation in early pregnancy. Maternal serum levels are relatively high in the first trimester, but falls after pregnancy week 10-11, suggesting an essential role for PROK1 in early pregnancy.[3] In early pregnancy, PROK1 promotes the proliferation of cytotrophoblasts at the expense of their differentiation and by this contributes to the formation and maintenance of trophoblastic plugs in the maternal spiral arteries that protects the developing foetus and placenta from highly oxygenated maternal blood. At week 10-11, the decrease in circulating and placental levels of PROK1 possibly contributes to differentiation and invasion of extravillous trophoblasts into the decidua and remodelling the maternal spiral arteries to ensure sufficient amount of oxygen and nutrients for the growing foetus.[2] Dysregulation of PROK1 has been associated with placenta-related pregnancy complications, such as pre-eclampsia and intrauterine growth restriction.[2,3,4].
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