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Prostacyclin Pathway Shown to Drive Fetal Membrane Repair in Preclinical Study

Mouse models plus human cell data highlight IP receptor signaling as a potential target to curb pPROM-related preterm birth.

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.