Altered mRNA abundance of ASB15 and four other genes in skeletal muscle following administration of beta-adrenergic receptor agonists.

Beta-adrenergic receptor agonists (BA) stimulate skeletal muscle growth. However, downstream signaling pathways that facilitate this effect remain poorly defined. Objectives of this study were to identify genes differentially expressed after administration of a novel BA and to evaluate the expression of one of those genes in additional models of skeletal muscle growth. Differentially expressed gene fragments were identified through differential display of skeletal muscle biopsies from five steers 24 h after administration of the BA. Five gene fragments designated DD53, DD143, DD163, DD209, and DD214 were identified. Tissue distribution of these genes was evaluated by RT-PCR. While DD53, DD163, DD209, and DD214 were expressed across tissues, DD143 mRNA expression was most abundant in skeletal muscle. DD143, later identified as bovine ASB15, was evaluated in rats following administration of anabolic compounds. Thirteen 7-wk-old female rats were randomly assigned to each of four treatment groups including: control, clenbuterol, trenbolone acetate (TBA), and growth hormone (GH). Changes in rat Asb-15 mRNA were measured at 30 min, 12 h, and 24 h following intraperitoneal injections of each compound. Clenbuterol treatment decreased Asb-15 mRNA in skeletal muscle at 12 and 24 h (P < 0.01) and also decreased mRNA in lung at 12 h (P < 0.05). TBA and GH treatments did not alter Asb-15 mRNA in any of the tissues evaluated (P > 0.10). These results are the first to associate an Asb gene family member with muscle growth or BA administration and suggest a potential role for ASB15 in beta-agonist-induced skeletal muscle hypertrophy.