The Research About Effect Of Angâ…¡ On The Invasion Of Trophoblast Cells

Background and Objective:Pre-eclampsia is unique to human pregnancy and the leading cause of maternal and perinatal deaths .At present ,the pathogeny is still unclear,so it's difficult to prevent and cure this disease. Lots of researches indicate that angiotensin II (Ang II) and its subtype 1 receptor(AT1R) are important in the pathogenesis of pre-eclampsia.The increased Ang II or the enhanced combination with AT1R participates in the pathogenesis of pre-eclampsia through effect on the placentation and spiral arteries remodeling. Valsartan,a selective inhibitor of AT1R,can resist hypertension efficiently. But it need to be researched whether it can be used to cure preeclampsia.Reduced trophoblast invasion is the key link to pathogenesis of preeclampsia. Although there is a study find that trophoblast invasion is reduced significantly with Ang II-treated cells after 24h,many reseatches test that Ang II stimulates several key protein tyrosine kinases including focal adhesion kinase (FAK) that activate cellular proliferation, migration and adhesion of vascular smooth muscle cells and vascular endothelial cells et al.Focal adhesion kinase (FAK) play a key role in the signal transduction to mediate the cell invasion/migration. Phosphorylation of Tyr-397 in the cytosolic FAK is the key position to mediate the cell migration,which is low expression in the cytotrophoblast (CTB)of preeclampsia. There is no report whether Ang II regulate trophoblast invasion through FAK-associated signal pathway.Using the preeclamptic rats model induced by cold–stress stimulation, we study prevention and cure of preeclampsia and the expression of FAK(tyr397) in placenta with valsartan-pretreated. To culture the human trophoblast cells and study the effect of Ang II on the trophoblast invasion,then we'll discuss the FAK signal transduction of Ang II regulating trophoblast invasion.These could provide certain help for pathogenesis and prevention and cure of preeclampsia.