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Gene expression kinetics of muscle-specific micro-RNAs (miR-1, miR-133, and miR-206) and atrogenes (MuRF1 and MAFbx) in cells treated in vitro with TNF-alpha and INF-gamma.

Grant number: 12/10539-1
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): September 01, 2012
Effective date (End): December 31, 2013
Field of knowledge:Biological Sciences - Morphology - Histology
Principal researcher:Robson Francisco Carvalho
Grantee:Carlos Augusto Barnabe Alves
Home Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil
Associated scholarship(s):13/00477-1 - Biogenesis control of induced pluripotent stem Cells-Specific microRNAs, BE.EP.IC


The skeletal muscle atrophy is a common phenomenon in many chronic systemic diseases such a sepsis, chronic heart failure, chronic obstructive pulmonary disease, chronic kidney disease, diabetes, AIDS and cancer. These diseases may be accompanied by a complex metabolic syndrome characterized by muscle wasting, denominated cachexia. The molecular pathways responsible for cachexia are not completely understood, however, evidence suggest that pro-inflammatory cytokines like Tumor Necrosis Factor (TNF)-± and Interferon (INF)-³ have a key role in molecular pathways related to loss of function and muscle mass. The complexity of mechanisms controlling gene expression in this process suggests the involvement of additional regulatory molecules, such as microRNAs; these RNA molecules encoded by the genome regulate the function of skeletal muscle during development and various muscle diseases. MicroRNAs orchestrate common pathways or biological function, this unique feature gives rise as an effective tool for determining the pathways involved in specific diseases or biological processes. The hypothesis of this work is that muscle atrophy induced by TNF-± and INF-³ changes the kinetics of expression i) of Myod and Myogenin with alteration in the expression profile of muscle-specific micro-RNAs miR-1, miR-133, and miR-206.

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