Placenta · 2026
Placental endoglin protein expression across gestation in normal pregnancy and preeclampsia: Implications for anti-angiogenic therapeutic strategies.
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Basu Jayasri, Armstrong Ashley, Uzianbaeva Liaisan, Mehdizadeh Alireza, Mikhail Magdy
Аннотация
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.
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.