Role of Progesterone Membrane Receptors in the Pathogenesis of Preeclampsia

Preeclampsia affects approximately 3-8% of pregnancies and is characterized by new-onset hypertension and multisystem involvement after 20 weeks of gestation. Despite extensive research, its molecular pathogenesis remains incompletely understood.

Progesterone is essential for successful pregnancy maintenance and contributes to uterine quiescence, trophoblast function, and maternal-fetal immune tolerance. In addition to classical genomic signaling pathways, progesterone exerts rapid non-genomic effects through membrane-associated receptors, including PGRMC1, PGRMC2, and PAQR family members.

Recent studies have demonstrated that these receptors are involved in trophoblast invasion, angiogenesis, endothelial function, and inflammatory regulation. Alterations in their expression may contribute to abnormal placentation and endothelial dysfunction observed in preeclampsia.

The present study will evaluate placental expression levels of PGRMC1, PGRMC2, and selected PAQR family receptors in women with preeclampsia and healthy controls. Placental tissue obtained after delivery will undergo immunohistochemical and mRNA expression analyses. The findings may improve understanding of the molecular mechanisms underlying preeclampsia and identify potential biomarkers or therapeutic targets.

Inclusion criteria

Preeclampsia Group Women aged 18-45 years Singleton pregnancy Diagnosis of preeclampsia according to ACOG criteria Delivery at the study center Written informed consent Control Group Women aged 18-45 years Singleton pregnancy Normotensive healthy pregnancy Delivery at the study center Written informed consent

Exclusion criteria

Age <18 or >45 years Multiple gestation Fetal structural or chromosomal anomalies Chronic hypertension Pre-existing diabetes mellitus Autoimmune diseases Renal disease Other major systemic disorders

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