AI Summary & Key Takeaways
AI InsightIn addition, the expression of CD68 was found to be markedly increased in preeclamptic placentas in comparison to control placentas.Conclusion: The increased expression of E-cadherin, endothelin-1, and CD68 may play an important role in impaired trophoblast invasion, endothelial dysfunction, and inadequate spiral remodeling, which are key factors involved in the pathogenesis of PE.
📌 3 Key Takeaways
Abstract
Objective: Preeclampsia (PE) is a complex pregnancy-specific disorder characterized by the onset of hypertension and proteinuria in the second trimester of pregnancy. The pathogenesis of PE still remains unknown. Revealing the specific proteins involved in placental functions is important for a better understanding of the pathogenesis of PE. In this study, we aimed to investigate the expression levels of E-cadherin, endothelin-1, and CD68 in both preeclamptic and normal placentas.Materials and Methods: In this study, placentas after birth at 35-38 weeks were included. Ten preeclamptic placentas and 10 normal placentas were used. The expression levels of E-cadherin, endothelin-1, and CD68 were measured by western blot. Results: It was observed that the expression of E-cadherin and endothelin-1 was not at detectable levels in normal placentas; however, E-cadherin and endothelin-1 were observed to be highly expressed in preeclamptic placentas. In addition, the expression of CD68 was found to be markedly increased in preeclamptic placentas in comparison to control placentas.Conclusion: The increased expression of E-cadherin, endothelin-1, and CD68 may play an important role in impaired trophoblast invasion, endothelial dysfunction, and inadequate spiral remodeling, which are key factors involved in the pathogenesis of PE.