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Time-course changes of catabolic proteins following muscle atrophy induced by dexamethasone

Authors :
Lidiane M. Souza
Aline Mio Martuscelli
Paula B. Constantino
Anderson Saranz Zago
Sandra Lia do Amaral
Anderson G. Macedo
James W. E. Rush
Andre L. O. Krug
Carlos Ferreira dos Santos
Universidade Estadual Paulista (Unesp)
University of Waterloo
Universidade de São Paulo (USP)
Source :
ResearcherID, Scopus, Repositório Institucional da UNESP, Universidade Estadual Paulista (UNESP), instacron:UNESP
Publication Year :
2015

Abstract

Made available in DSpace on 2018-12-11T17:23:03Z (GMT). No. of bitstreams: 0 Previous issue date: 2016-03-01 Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) This study was designed to describe the time-course changes of catabolic proteins following muscle atrophy induced by 10 days of dexamethasone (DEX). Rats underwent DEX treatment for 1, 3, 5, 7 and 10 days. Body weight (BW) and lean mass were obtained using a dual energy X-ray absorptiometry (DEXA) scan. Muscle ringer finger1 (MuRF-1), atrogin-1 and myostatin protein levels were analyzed in the tibialis anterior (TA), flexor hallucis longus (FHL) and soleus muscles. DEX treatment reduced lean mass since day-3 and reduced BW since day-5. Specific muscle weight reductions were observed after day-10 in TA (-23%) and after day-5 in FHL (-16%, -17% and -29%, for days 5, 7 and 10, respectively). In TA, myostatin protein level was 36% higher on day-5 and its values were normalized in comparison with controls on day-10. MuRF-1 protein level was increased in TA muscle from day-7 and in FHL muscle only on day-10. This study suggests that DEX-induced muscle atrophy is a dynamic process which involves important signaling factors over time. As demonstrated by DEXA scan, lean mass declines earlier than BW and this response may involve other catabolic proteins than myostatin and MuRF-1. Specifically for TA and FHL, it seems that myostatin may trigger the catabolic process, and MuRF-1 may contribute to maintain muscle atrophy. This information may support any intervention in order to attenuate the muscle atrophy during long period of treatment. Joint Graduate Program in Physiological Sciences PIPGCF UFSCar UNESP Department of Physiological Sciences Federal University of São Carlos - UFSCAR Department of Physical Education Universidade Estadual Paulista - UNESP Department of Kinesiology Faculty of Applied Health Sciences University of Waterloo Department of Biological Sciences Bauru School of Dentistry University of São Paulo USP Joint Graduate Program in Physiological Sciences PIPGCF UFSCar UNESP Department of Physiological Sciences Federal University of São Carlos - UFSCAR Department of Physical Education Universidade Estadual Paulista - UNESP CNPq: 130232/2011-4 FAPESP: 2012/03816-9 FAPESP: 2012/21820-3

Details

ISSN :
18785867
Volume :
107
Database :
OpenAIRE
Journal :
Steroids
Accession number :
edsair.doi.dedup.....d8d12a91d72d6a0540987d638e8fddcb