62-OR

Abstract

Objectives Autophagy is a lysosomal degradation pathway that removes protein aggregates and damaged organelles maintaining the cellular integrity. It is an inducible process that responds to the environment and it seems to be essential for cell survival during stress, starvation, hypoxia and consequently to the placenta implantation and development. Studies on the role of autophagy in placenta from pregnant women with preeclampsia are scarce and still unclear. The aim of this study was to compare the expression of autophagy-related proteins, LC3-II, beclin-1 as well as mTOR protein in placental tissue from pregnant women with preeclampsia and normotensive pregnant women. Methods The expression of LC3-II and beclin-1 proteins involved in the autophagosome formation as well as mTOR protein was evaluated in 18 placentas of pregnant women with preeclampsia and in 20 of normotensive pregnant women who had elective cesarean delivery before the onset of labor. Fragments of the placenta were obtained immediately after delivery and the samples were prepared for real-time quantitative polymerase chain reaction (RT-qPCR), immunohistochemistry and transmission electron microscopy analysis. Results LC3-II expression as detected by RT-qPCR was significant higher in placentas of normotensive pregnant women compared with preeclamptic women. No significant difference in beclin-1 and mTOR expression was seen between these two groups. LC3-II, beclin-1 and mTOR proteins were detected by immunohistochemistry in syncytiotrophoblast and cytotrophoblast in both groups, and the presence of autophagic vacuoles containing intracytoplasmatic organelles was confirmed with electron microscopy. Conclusions The results of the impaired autophagy demonstrated by decrease of LC3- II expression in placenta of preeclamptic patients might play a role in the pathophysiology of preeclampsia. Financial support: FAPESP 2013/00535-1 and 2012/24697-8. Disclosures I.C. Weel: None. V.R. Ribeiro: None. M. Romao: None. M.L. Matias: None. V.T. Borges: None. J.C. Peracoli: None. J.P. Araujo Jr: None. M.T. Peracoli: None.