Progestin-indusced decidualisation promotes human endometrial haemostasis and vascular stabulity

This chapter focuses on the role of progestin-induced decidualisation in regulating endometrial haemostasis and vascular stability. Observations made by in situ hybridisation and immunohistochemistry of endometrial sections, together with in vitro studies of human endometrial stromal cells (HESCs), indicate that progest-ininduced decidualisation creates a pro-haemostatic, vascular-stabilising milieu that resists bleeding. During decidualisation of human endometrium, the interstitial-type extracellular matrix (ECM) of the follicular phase, which is enriched in fibronectin and collagen types I, III,V and VI, is converted to a mixture of residual interstitial proteins and new peridecidual basal laminar-type components. The resulting peridecidual cell ECM plays an integral role in implantation by modulating migration of the invading trophoblast and in counteracting the threat of local haemorrhage during endovascular trophoblast invasion by serving as a vascular support and stabilising scaffolding structure. Uterine natural killer (NK) cells have been implicated in maintaining decidualisation and in limiting trophoblast invasion.