Evaluation of epigenetic status of miRNA markers for Multiple Sclerosis.

• Grant number: 12/15746-5
• Support Opportunities: Scholarships abroad - Research Internship - Doctorate
• Start date: October 10, 2012
• End date: March 09, 2013
• Field of knowledge: Biological Sciences - Genetics - Human and Medical Genetics
• Principal Investigator: Wilson Araújo da Silva Junior
• Grantee: Julio Cesar Cetrulo Lorenzi
• Supervisor: Maja Jagodic
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Institution abroad: Karolinska Institutet, Sweden
• Associated to the scholarship: 10/00310-1 - miRNA signature of T lymphocyte subpopulations from healthy and multiple sclerosis patients, BP.DR

Abstract

Multiple Sclerosis (MS) is an inflammatory disease that occurs in the central nervous system and is characterized by a perivenular lymphocytic infiltrate, demyelination and variable axonal loss. The myelin sheath proteins are considered the main targets of attack for the T lymphocytes. MS perpetuation and induction evidences indicates that autoreactive T CD4+ have a central role in autoimmune pathogenesis of MS. The regulation of gene expression in these cells appears to have a direct connection in the development of MS. Among the different classes of molecules capable to regulate the gene expression, the microRNA (miRNAs) have been described with great importance in the autoimmune diseases. MiRNAs are small non-coding RNAs that are distributed in the human genome and controls the gene expression by the degradation of messenger RNA. Partial results from the researcher PhD. project, that aims to evaluate the miRNA expression in different T CD4+ e CD8+ lymphocyte subpopulations shows a miRNA signature that could be evolved in the physiopathology of MS. In order to investigate the control mechanisms of miRNA expression we propose, in collaboration with Dr. Maja Jagodic from Karolinska Institute (Stockholm, Sweden), to study the role of methylation in the epigenetic control of expression of some miRNAs that are differentially expressed in the MS patients.