Prostaglandin E2 and Its Role in Placenta Accreta Spectrum: A Literature Review

Tin Elasari (Doctorate in Biomedical Science, Faculty of Medicine, Universitas Sriwijaya, Sumatera Selatan)
Krisna Murti (Department of Anatomical Pathology, Faculty of Medicine, Universitas Sriwijaya/Mohammad Hoesin Hospital Palembang)
Erry Gumilar Dachlan (Department of Obstetrics and Gynecology, Faculty of Medicine, Universitas Airlangga/Dr. Soetomo Regional Hospital Surabaya)
Iche Andriyani Liberty (Department of Epidemiology and Biostatistics, Faculty of Public Health, Universitas Sriwijaya, Sumatera Selatan)
Rozi Aditya Aryananda (Department of Obstetrics and Gynecology, Faculty of Medicine, Universitas Airlangga/Dr. Soetomo Regional Hospital Surabaya)

Electronic Journal of Education, Social Economics and Technology
Vol 7, No 1 (2026)

Placenta accreta spectrum results in significant morbidities. Implantation process is regulated by PGE2 among other factors. This review aimed to discuss the role of PGE2 in the placenta accreta spectrum. Review of literatures searched in PubMed, PubMedCentral, EuropePMC, Wiley, and Science Direct with relevant keywords. Articles found were screened by authors and voted for inclusion. PGE2 is synthesized from arachidonic acid by COX. Increased synthesis of PGE2 results in increased angiogenesis and placental invasion. PGE2 action mainly occurs through the EP1-EP4 as the main receptors of PGE2. Reduced PGE2 receptors expression may results in defective decidualization resulting in poor pregnancy outcomes. Inactivation of PGE2 occurs through HPGD enzyme. Upregulation of HPGD results in lower PGE2 tissue concentration leading to decreased PGE2 activity. Disorders of HPGD expression has been implicated in abnormal implantation in animals. PGE2 synthesis, signaling, and inactivation plays significant role in placental invasion. Defects in any of the processes may lead into placenta accreta spectrum.