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Centre National de la Recherche Scientifique (A.H.C., D.D., M.H.M.-S., M.R., G.M.), Unité Mixte de Recherche 5123, Claude Bernard-Lyon 1 University, F69622 Villeurbanne, France; and Institute National de la Santé et de la Recherche Médicale (S.J.), Unité U413, University of Rouen, F76821 Mont-Saint-Aignan, France
Address all correspondence and requests for reprints to: Dr. G. Morel, Physiologie Intégrative, Cellulaire et Moléculaire, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5123, Université Claude Bernard-Lyon 1, Bâtiment R. Dubois, 43 Boulevard du 11 Novembre 1918, F69622 Villeurbanne cedex, France. E-mail: Gerard. Morel{at}univ-lyon1.fr.
Biological actions of GH on muscle growth and metabolism are mediated through specific trans-membrane receptors. The aim of this study was to determine GH receptor (GHR) mRNA expression in muscle atrophy. GHR gene expression in the rat was investigated by in situ hybridization and RT-PCR in slow-twitch oxidative muscle [soleus (SOL)] and fast-twitch glycolytic muscle [extensor digitorum longus (EDL)] after 7 and 35 d of hindlimb unloading. In control rats, the RT-PCR mRNAs levels of GHR were greater (+34%) in EDL compared with SOL. At single fiber level, relative expression of GHR mRNA increases in the following order: IIb>IIa>I. After hindlimb unloading, GHR expression significantly increased in atrophied SOL muscle after 7 (+170%) and 35 (+220%) d, whereas no significant alterations appeared in the EDL muscle. At the individual fiber level, in situ hybridization demonstrated this increase was accounted for by an increase in type I fiber expression of GHR transcripts. This increase was also seen in the EDL, but the low content of type I fibers in EDL resulted in a nonsignificant increase in GHR transcript content. The present data suggest that muscle atrophy is associated with a muscle fiber type-specific GHR mRNA up-regulation mechanism that helps protect atrophying fibers in EDL but might be part of an attempt to repair in SOL.
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