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Updated: Jan 26, 2026
Cryosectioning of Contiguous Regions of a Single Mouse Skeletal Muscle for Gene Expression and Histological Analyses
Published on: December 12, 2016
Arrdc2 and Arrdc3 elicit divergent changes in gene expression in skeletal muscle following anabolic and catabolic
Bradley S Gordon1,2, Michael L Rossetti1, Alexey M Eroshkin3,4
1Department of Nutrition, Food & Exercise Sciences, Florida State University , Tallahassee, Florida.
Abstract:
Skeletal muscle is a highly plastic organ regulating various processes in the body. As such, loss of skeletal muscle underlies the increased morbidity and mortality risk that is associated with numerous conditions. However, no therapies are available to combat the loss of muscle mass during atrophic conditions, which is due in part to the incomplete understanding of the molecular networks altered by anabolic and catabolic stimuli. Thus, the current objective was to identify novel gene networks modulated by such stimuli. For this, total RNA from the tibialis anterior muscle of mice that were fasted overnight or fasted overnight and refed the next morning was subjected to microarray analysis. The refeeding stimulus altered the expression of genes associated with signal transduction. Specifically, expression of alpha arrestin domain containing 2 (Arrdc2) and alpha arrestin domain containing 3 (Arrdc3) was significantly lowered 70-85% by refeeding. Subsequent analysis showed that expression of these genes was also lowered 50-75% by mechanical overload, with the combination of nutrients and mechanical overload acting synergistically to lower Arrdc2 and Arrdc3 expression. On the converse, stimuli that suppress growth such as testosterone depletion or acute aerobic exercise increased Arrdc2 and Arrdc3 expression in skeletal muscle. While Arrdc2 and Arrdc3 exhibited divergent changes in expression following anabolic or catabolic stimuli, no other member of the Arrdc family of genes exhibited the consistent change in expression across the analyzed conditions. Thus, Arrdc2 and Arrdc3 are a novel set of genes that may be implicated in the regulation of skeletal muscle mass.
Insights
Researchers identified two novel genes, alpha arrestin domain containing 2 (Arrdc2) and 3 (Arrdc3), that may regulate skeletal muscle mass. Their expression changes with stimuli promoting or suppressing muscle growth, suggesting a role in muscle plasticity.
Area of Science:
- Molecular Biology
- Physiology
- Genetics
Background:
- Skeletal muscle's plasticity is crucial for bodily functions, and its loss increases morbidity and mortality risks.
- Current therapies for muscle-wasting conditions are limited due to an incomplete understanding of underlying molecular networks.
- Identifying novel regulatory genes is essential for developing effective treatments for muscle atrophy.
Purpose of the Study:
- To identify novel gene networks modulated by anabolic and catabolic stimuli in skeletal muscle.
- To investigate the role of alpha arrestin domain containing 2 (Arrdc2) and alpha arrestin domain containing 3 (Arrdc3) in muscle mass regulation.
Main Methods:
- Microarray analysis of tibialis anterior muscle RNA from mice under different conditions (fasting, refeeding, mechanical overload, testosterone depletion, aerobic exercise).
- Quantitative analysis of Arrdc2 and Arrdc3 gene expression changes in response to various stimuli.
Main Results:
- Refeeding significantly lowered Arrdc2 and Arrdc3 expression (70-85%).
- Mechanical overload also reduced Arrdc2 and Arrdc3 expression (50-75%), with synergistic effects when combined with nutrients.
- Testosterone depletion and aerobic exercise increased Arrdc2 and Arrdc3 expression.
- Arrdc2 and Arrdc3 showed consistent, reciprocal expression changes across anabolic and catabolic conditions, unlike other Arrdc family members.
Conclusions:
- Arrdc2 and Arrdc3 represent a novel set of genes potentially involved in regulating skeletal muscle mass.
- These genes' expression patterns suggest a role in mediating responses to anabolic and catabolic stimuli.
- Further research into Arrdc2 and Arrdc3 could uncover new therapeutic targets for muscle-wasting diseases.
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