| Grant number: | 13/10633-0 |
| Support Opportunities: | Regular Research Grants |
| Start date: | October 01, 2013 |
| End date: | March 31, 2016 |
| Field of knowledge: | Biological Sciences - Morphology - Anatomy |
| Principal Investigator: | Renato Ferretti |
| Grantee: | Renato Ferretti |
| Host Institution: | Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil |
Abstract
In Duchenne muscular dystrophy (DMD) and in the mdx mice, the experimental model of DMD, the lack of dystrophin leads to muscle necrosis and progressive cardiorespiratory failure. The absence of dystrophin leads to a decrease in expression of dystrophin-glycoprotein complex (DGC) and loss of homeostasis of calcium (Ca2+), resulting in myonecrosis. MicroRNAs (miRs), non-coding RNAs, appear to coordinate the signaling pathways that predispose to muscle fiber necrosis. Studies showed that the intrinsic laryngeal muscles (ILM) are protected from myonecrosis, probably because they had normal levels of components of the DGC and better ability to regulate calcium. In the present study, we will investigate whether the miRs are involved in protecting against myonecrosis in mdx mice. We will carry out a comparative study of the pathways that regulate the expression of components that help stabilizes the sarcolemma and are involved in Ca2+ homeostasis in dystrophic spared and affected muscles. Additionally, we will evaluate the effect of therapy with eicosapentaenoic acid (EPA) in the expression of these miRs and their correlation with protection against myonecrosis in dystrophinopathies. This project will offer new mechanistic insights into the pathophysiology of dystrophinopathies opening new perspectives of therapies for DMD. (AU)
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