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Evaluation of autophagy in placenta of pregnant women with pre-eclampsia

Grant number: 13/03872-9
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): May 01, 2013
Effective date (End): December 31, 2014
Field of knowledge:Health Sciences - Medicine - Maternal and Child Health
Principal researcher:Maria Terezinha Serrão Peraçoli
Grantee:Vanessa Rocha Ribeiro Vasques
Home Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil

Abstract

Preeclampsia (PE) is a syndrome that affects between 5% and 7% of pregnancies and is a leading cause of morbidity and mortality, both maternal and fetal. It is a systemic disease characterized by multiple changes in the mother and clinically identified by hypertension and proteinuria, which arise after the 20th week of gestation. Placental hypoxia is an initial factor in PE, due to the low uteroplacental blood flow. Thus, the placenta plays an essential role in this disease, since problems in placentation process culminate in reduced blood perfusion and therefore hypoxic / ischemic placenta as well as intrauterine fetal growth restriction. Autophagy, a lysosomal degradation pathway, removes protein aggregates and damaged organelles maintaining cellular integrity. This pathway may be compromised in pregnant women with PE, since it is observed the presence of placental lesions caused by hypoxia / ischemia. This project aims to determine the occurrence of autophagy in placenta of pregnant women with PE. Forty pregnant women will be studied, being 20 normotensive and 20 with preeclampsia. Fragments of placenta including maternal and fetal sides, will be obtained immediately after delivery. Each fragment will be cut into two equal parts, one being placed in buffered formalin for immunohistochemistry analysis, and another part will be frozen in liquid nitrogen for subsequent homogenate preparation for Western blot analysis. The occurrence of autophagy will be determined by quantifying LC3, Beclin-1 and mTOR by immunohistochemistry and Western blot. (AU)

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