Effects of dexamethasone on the expression of beta(1)-, beta (2)- and beta (3)-adrenoceptor mRNAs in skeletal and left ventricle muscles in rats.
Glucocorticoids are known to increase the density and mRNA levels of beta-adrenoceptors (beta-AR) via the glucocorticoid receptor (GR) in many tissues. However, the effects of these changes in the skeletal and cardiac muscles remain relatively unknown. We have investigated the effects of dexamethasone on the expression of the beta(1)-, beta(2)-, and beta(3)-AR mRNAs and GR mRNA in fast-twitch fiber-rich extensor digitorum longus (EDL), slow-twitch fiber-rich soleus (SOL), and left ventricle (LV) muscles by real-time quantitative RT-PCR. Male rats were divided into a dexamethasone group and control group. The weight, RNA concentration, and total RNA content of EDL muscle were 0.76-, 0.85-, and 0.65-fold lower, respectively, in the dexamethasone group than in the control group. The weight, RNA concentration, and total RNA content of SOL muscle were 0.92-, 0.87-, and 0.81-fold lower, respectively, in the dexamethasone group than in the control group; these differences were significant. However, the weight/body weight and total RNA content/body weight of LV muscle were 1.38- and 1.39-fold higher, respectively, in the dexamethasone group than in the control group, respectively; these differences were also significant. Dexamethasone significantly decreased GR mRNA expression in EDL muscle without changing the expression of the beta(1)-, beta(2)-, and beta(3)-AR mRNAs. However, dexamethasone significantly decreased the expressions of beta(2)-AR and GR mRNAs in SOL muscle and significantly increased beta(1)-AR mRNA expression in LV muscle-without changing GR mRNA expression. These results suggest that the effects of dexamethasone on the expression of beta(1)- and beta(2)-AR mRNAs and muscle mass depend on the muscle contractile and/or constructive types.
Kawano
Fuuun
F
Laboratory of Physiological Sciences, Faculty of Human Sciences, Waseda University, 2-579-15 Mikajima, Tokorozawa, Saitama, 359-1192, Japan.
Tanihata
Jun
J
Sato
Shogo
S
Nomura
Sachiko
S
Shiraishi
Akira
A
Tachiyashiki
Kaoru
K
Imaizumi
Kazuhiko
K
D000818:Animals; D001835:Body Weight / Q000502:physiology; D003907:Dexamethasone / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004326:Drinking / Q000502:physiology; D004435:Eating / Q000502:physiology; D005938:Glucocorticoids / Q000494:pharmacology; D006352:Heart Ventricles / Q000378:metabolism*; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018342:Receptors, Adrenergic, beta-1 / Q000187:drug effects / Q000378:metabolism*; D018343:Receptors, Adrenergic, beta-2 / Q000187:drug effects / Q000378:metabolism*; D022702:Receptors, Adrenergic, beta-3 / Q000187:drug effects / Q000378:metabolism*
D005938:Glucocorticoids; D012333:RNA, Messenger; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D022702:Receptors, Adrenergic, beta-3; D003907:Dexamethasone