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Dicer deletion in adipocytes and its influence in cardiovascular diseases

Grant number: 12/06238-6
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): June 01, 2012
Effective date (End): December 31, 2012
Field of knowledge:Biological Sciences - Physiology
Principal Investigator:Marcelo Alves da Silva Mori
Grantee:Adriano Silva Martins
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Research Proposal - Postdoctoral Fellowship - FAPESP Title: "Dicer Deletion in Adipocytes and Its Influence in Cardiovascular Diseases"Postdoctoral Candidate: Dr. Adriano Silva MartinsSupervisor: Dr. Marcelo Alves da Silva MoriInstitution: Biophysics Department - Federal University of Sao PauloDate:April, 2012 AbstractAging process and hypercaloric diet contribute to chronic diseases development, which can result in a cluster of metabolic and cardiovascular symptoms called "metabolic syndrome". Among these symptoms, stands the atherosclerosis, which is characterized by the formation of fat plaques with partial or total occlusion of the arteries lumen. Our data shows that the processing of miRNAs is diminished with the aging process in mice adipose tissue, and that this process can be reversed by caloric restriction. Adipose tissue has the potential to secrete molecules that may regulate the function of other tissues, participating actively in cardiovascular diseases genesis. Our previous data allow us to formulate the hypothesis that the reduction of miRNAs processing in adipose tissue can promote premature risk of age-related diseases, particularly cardiovascular diseases. With this in view, we will study animals (mice) unable to produce miRNAs in fat tissue-specific given the gene deletion that encodes Dicer, an enzyme critical towards mature miRNAs processing. Preliminary data show an elevation in serum levels of lipids and change to some hormones secretion that are involved in the metabolism of fats and carbohydrates in these animals, suggesting an environment favourable to the development of atherosclerosis. In this project we will challenge these mice with a Western diet rich in fats and/or infusion of Angiotensin II in pressor dose and/or a loss of function mutation in the gene apoE, and we will assess the development of atheroma plaques, plus serum metabolic profile in such animals. Our goal is to understand how the processing of miRNAs in adipose tissue controls the genesis of age-related diseases, identifying a new mechanism in the pathogenesis of atherosclerosis

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