Placental endoglin protein expression across gestation in normal pregnancy and preeclampsia: Implications for anti-angiogenic therapeutic strategies.

INTRODUCTION

Preeclampsia is a human-specific hypertensive disorder of pregnancy characterized by new-onset hypertension and proteinuria after 20 weeks of gestation. Placental dysfunction and angiogenic imbalance are central to its pathophysiology. Endoglin, a membrane-bound glycoprotein and precursor of soluble endoglin (sEng), contributes to impaired placentation. This study examined placental endoglin protein expression across normal gestation and compared it with expression in preeclampsia.

METHODS

Placentas from normotensive pregnancies across all three trimesters and from women with preeclampsia were collected under IRB-approved protocols. Chorionic villi were isolated, and endoglin protein expression was quantified using a monoclonal anti-human Endoglin/CD105 ELISA kit, DY1097. Of a total of 333 placentas, 324 with gestational age ≥37-weeks comprised the primary dataset, and 9 preeclamptic placentas delivered before 37 weeks were analyzed separately. Group differences were assessed using ANOVA, with significance set at p < 0.05.

RESULTS

Endoglin protein expression varied significantly across gestation (p < 0.001). Mean levels (ng/100 mg tissue) were: first trimester 40.94 (n = 116), second trimester 29.24 (n = 79), and third trimester 30.93 (n = 100). Preeclamptic placentas exhibited markedly higher levels (50.77; n = 29). Expression patterns were comparable between Black American and Hispanic women.

DISCUSSION: Placental endoglin protein expression peaks in early gestation and is significantly upregulated in preeclampsia. These findings support the role of angiogenic imbalance in disease pathogenesis and provide a biological marker distinguishing normal from pathological placentation. The data also offer a foundation for estimating early pregnancy sEng levels, which may inform dosing strategies for future monoclonal antibody therapies targeting sEng.