ABSTRACT
Preeclampsia is caused by the dysfunction of placental trophoblast infiltration.The trophoblast immersed in endometrial layer shallow (only up to decidua layer),concurrently resulted in uterine vascular remodeling disorder,and cause placental tissue ischemia,hypoxia,and a series of clinical manifestations of preeclampsia.Rho is a guanosine triphosphate-binding protein whose downstream molecule is Rho-associated coiled-coil forming protein kinase (Rock).Recent studies suggest that Rho/Rock signaling pathway,by regulating the polymerization state of intracellular microfilament skeleton,affects the behavior and function of cells,such as cell adhesion,migration,cell contraction,infiltration and transformation of cancer cells,etc.Thus is involved in the pathogenesis of many diseases.This article summarized the progress of research in the influence of trophoblast infiltration capacity,activation,regulation and the relationship with pregnancy of Rho/Rock signaling pathway,to provide reference for clinical research.
ABSTRACT
Objective To investigate expressions of Ras homologue protein family A (RhoA)/RhoB and Rho-associated coiled coil Rho forming protein Kinase 1 (Rock1)/Rock2 in placenta tissues of severe preeclampsia (sPE) to clarify the molecular mechanisms of sPE.Methods The locations and expressions of RhoA/RhoB and Rock1/Rock2 between two groups were detected with immunohistochemistry.Results RhoA,RhoB,Rock1,and Rock2 were mainly distributed in cytoplasms of syncytiotrophoblasts,cytotrophoblast,endothelial cells,and endometrial stromal cells.Rock1 and Rock2 were less expressed in nucleus.The expression levels of RhoA,RhoB,Rock1,and Rock2 in sPE group were significantly higher than control group (P ＜ 0.05).Conclusions The signal pathway that consists of upstream RhoA/RhoB and downstream Rock1/Rock2 is up-regulated in sPE.It demonstrates that signal molecules including RhoA,RhoB,Rockl,and Rock2 may involve in the sPE pathogenesis through affecting shallow placenta implantation in preeclampsia,ischemia,hypoxia and apoptosis of trophoblasts,and injury of vascular endothelial cells and artery vasospasm.