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Protein quality control in dysfunctional/atrophic skeletal muscle: roke of B2 adrenoceptor

Grant number: 15/50429-9
Support type:Regular Research Grants
Duration: June 01, 2016 - May 31, 2018
Field of knowledge:Biological Sciences - Physiology
Cooperation agreement: University of California, Davis (UC Davis)
Mobility Program: SPRINT - Projetos de pesquisa - Mobilidade
Principal Investigator:Julio Cesar Batista Ferreira
Grantee:Julio Cesar Batista Ferreira
Principal investigator abroad: Sue Carol Bodine
Institution abroad: University of California, Davis (UC Davis), United States
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated research grant:15/20783-5 - Protein quality control in dysfunctional/atrophic skeletal muscle: role of b2-adrenoceptor, AP.R


Our current results demonstrate that intracellular protein quality control [machinery that detects, repairs and disposes cytotoxic proteins] is impaired during muscle dysfunction and wasting. We also show that pharmacological activation of β2-adrenoceptor induces an overall improvement of protein quality control-related mechanisms in skeletal muscle. Our next step is to establish a causal relationship between 112-adrenoceptor activation and improved protein quality control in skeletal muscle. We expect that disruption of intracellular protein quality control components such as proteasome and lysosome will abolish the benefits off12- adrenoceptor activation in a rodent model of sciatic nerve constriction. Although we use an animal model of muscle dysfunction induced by neural trauma, our rationale could be useful for other skeletal muscle disorders related to disrupted intracellular protein quality control such as muscular dystrophies and aging. (AU)