Casse Al Hassan, Desplanches Dominique, Mayet-Sornay Marie Hélène, Raccurt Mireille, Jegou Sylvie, Morel Gérard
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5123, Claude Bernard-Lyon 1 University, F69622 Villeurbanne, France.
Endocrinology. 2003 Aug;144(8):3692-7. doi: 10.1210/en.2003--0311.
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.
生长激素(GH)对肌肉生长和代谢的生物学作用是通过特定的跨膜受体介导的。本研究的目的是确定肌肉萎缩中生长激素受体(GHR)mRNA的表达情况。通过原位杂交和逆转录聚合酶链反应(RT-PCR),研究了后肢卸载7天和35天后,大鼠慢肌氧化肌[比目鱼肌(SOL)]和快肌糖酵解肌[趾长伸肌(EDL)]中GHR基因的表达。在对照大鼠中,EDL中GHR的RT-PCR mRNA水平比SOL高(+34%)。在单纤维水平上,GHR mRNA的相对表达按以下顺序增加:IIb>IIa>I。后肢卸载后,萎缩的SOL肌肉中GHR表达在7天(+170%)和35天(+220%)后显著增加,而EDL肌肉中未出现明显变化。在单纤维水平上,原位杂交表明这种增加是由于I型纤维中GHR转录本表达增加所致。在EDL中也观察到了这种增加,但EDL中I型纤维含量低导致GHR转录本含量增加不显著。目前的数据表明,肌肉萎缩与一种肌肉纤维类型特异性的GHR mRNA上调机制有关,该机制有助于保护EDL中萎缩的纤维,但可能是SOL中修复尝试的一部分。