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Alpha Arrestin Domain Containing 2 and Alpha Arrestin Domain Containing 3 Expression is Reduced in Skeletal Muscle by Anabolic Stimuli and Increased by Catabolic Stimuli
Author(s) -
Gordon Bradley Scott,
Rossetti Michael L,
Kimball Scot R
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.700.10
Subject(s) - anabolism , skeletal muscle , catabolism , endocrinology , medicine , stimulus (psychology) , arrestin , biology , gene expression , chemistry , microbiology and biotechnology , biochemistry , signal transduction , gene , metabolism , psychology , g protein coupled receptor , psychotherapist
Skeletal muscle is a highly plastic organ capable of increasing or decreasing in size depending upon the stimuli placed upon it. While this is known, the molecular factors that contribute to changes in skeletal muscle mass under anabolic and catabolic conditions remain ill defined. As such, the objective here was to identify novel genes that likely contribute to changes in skeletal muscle mass following anabolic or catabolic stimuli. For the initial identification of such genes, male mice were fasted overnight to induce a catabolic state in the skeletal muscle. The next morning, half of the mice were allowed to refeed for 30 minutes to effectively impart an anabolic stimulus on the skeletal muscle. Using an unbiased microarray approach and subsequent qRT‐PCR validation, the refeeding stimulus resulted in a significant reduction in the mRNA expression of Alpha Arrestin Domain Containing 2 (Arrdc2) and Alpha Arresting Domain Containing 3 (Arrdc3) in the tibialis anterior (TA) muscle. The reduction in Arrdc2 and Arrdc3 mRNA expression was not limited to nutrient consumption or the TA muscle as mechanical overload also reduced Arrdc2 and Arrdc3 expression in the TA and plantaris muscles. Moreover, the combination of nutrient consumption with mechanical overload had a synergistic effect on reducing Arrdc2 and Arrdc3 expression. Interestingly, these reductions in Arrdc2 and Arrdc3 expression following mechanical overload occurred even when signaling through the mechanistic target of rapamycin in complex 1 (mTORC1) growth pathway was disrupted. On the converse, Arrdc2 and Arrdc3 mRNA expression was increased in the muscle by catabolic stimuli other than fasting, which included androgen deprivation and the metabolic stress imposed by an acute bout of aerobic exercise. The divergent changes in Arrdc2 and Arrdc3 mRNA expression in the skeletal muscle following anabolic and catabolic stimuli were consistently related to the corresponding changes in markers of autophagy activation. While Arrdc2 and Arrdc3 expression showed consistent and divergent changes in expression under these conditions, no consistent changes in expression of other members of the Alpha Arresting Domain Containing family of genes were observed. In all, these data suggest changes in Arrdc2 and Arrdc3 expression may contribute to the regulation of skeletal muscle mass following anabolic and catabolic stimuli by altering autophagy activation. Support or Funding Information NIH‐DK15658 (SRK) and FSU Council on Research and Creativity (BSG) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .