Overview
- In The American Journal of Pathology, researchers report that prostacyclin signaling through the IP receptor promotes healing by stimulating amnion mesenchymal cell proliferation and migration.
- At rupture sites in a mouse model, prostaglandin pathway genes and prostacyclin production were locally upregulated alongside an increase in repair cell numbers.
- Pharmacologic IP receptor blockade impaired amnion repair, while treatment with an IP agonist partially restored healing capacity.
- IP-deficient mouse fetuses showed compromised membrane repair and fewer proliferating mesenchymal cells compared with wild-type controls.
- In cultured human amnion mesenchymal cells, IP activation enhanced proliferation and migration, supporting translational potential for pPROM but remaining at a preclinical stage.