Overexpression of EMT genes in endothelial cells during Endothelial Mesenchymal Transition

• Grant number: 10/51962-9
• Support Opportunities: Regular Research Grants
• Start date: January 01, 2011
• End date: December 31, 2012
• Field of knowledge: Biological Sciences - Genetics - Human and Medical Genetics
• Agreement: MIT
• Principal Investigator: Dimas Tadeu Covas
• Grantee: Dimas Tadeu Covas
• Principal researcher abroad: Robert Allan Weinberg
• Institution abroad: Massachusetts Institute of Technology (MIT), United States
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Endothelial Mesenchymal Transition (EndMT) is categorized as a specialized form of Epithelial Mesenchymal transition (EMT) that occurs in embryonic development during the formation of the heart valves and is considered one of the possible causes of fibrosis. There are some evidences that activated fibroblasts of the tumor stroma may derive from endothelial cells or its precursor cells that underwent an EndMT. The principal aim of this collaboration project is to investigate if endothelial cells (ECs) could generate mesenchymal cells (MSCs) through EndMT. For this purpose, EMT-related transcription factors will be overexpressed in ECs and we will verify whether they are able to induce an EndMT and, if the EndMT occurs, what is the role of these MSCs or mesenchymal-like cells in the tumor formation. In this regard, morphological, molecular and functional analysis will be conducted in these MSCs-derived ECs population. (AU)