New Research Reveals Essential Role of Prostacyclin in Fetal Membrane Repair to Prevent Preterm Birth

Recent scientific findings have shed light on the critical function of prostacyclin, a lipid signaling molecule, in the healing process of fetal membranes following rupture. When the amniotic membranes rupture prematurely, it often results in preterm birth, a leading cause of neonatal complications and infant mortality. Currently, effective treatments are limited, emphasizing the importance of understanding underlying healing mechanisms.

Published in The American Journal of Pathology, a groundbreaking study led by researchers from Kyoto University investigates how prostacyclin contributes to membrane repair. Using a mouse model of fetal membrane rupture, the study revealed that prostacyclin signaling through its receptor (IP) significantly enhances the proliferation and migration of amnion mesenchymal cells—key cells involved in wound healing. Elevated expression of genes responsible for prostaglandin and prostacyclin synthesis at the rupture sites indicates a natural reparative response.

The research demonstrated that inhibiting the prostacyclin receptor impairs membrane healing and decreases the number of proliferating mesenchymal cells, whereas activation of this receptor with specific agonists can partially restore the repair process. Additionally, genetically modified mice deficient in IP showed compromised healing, confirming prostacyclin's vital role. In vitro experiments with human amnion cells further supported these findings, showing increased cell proliferation and migration upon IP activation.

Lead author Dr. Masahito Takakura explains that prostacyclin's role extends beyond its conventional functions of relaxing blood vessels and preventing clotting. Its targeted synthesis at the rupture site appears to promote tissue regeneration, which could be harnessed for therapeutic interventions. Dr. Haruta Mogami emphasizes that this discovery offers new insights into fetal membrane healing mechanisms and could lead to novel treatments aimed at reducing preterm birth risks.

This research advances understanding of prostaglandin involvement in pregnancy, specifically highlighting the specific and significant role of prostacyclin in membrane repair. Future therapeutic strategies might focus on modulating prostacyclin signaling to facilitate healing after membrane rupture, ultimately helping to prevent preterm birth and improve neonatal outcomes.