Abstract
Skeletal muscle makes up approximately 40% of the total body mass, providing structural support and enabling the body to maintain posture, to control motor movements and to store energy. It therefore plays a vital role in whole body metabolism. Skeletal muscle displays remarkable plasticity and is able to alter its size, structure and function in response to various stimuli; an essential quality for healthy living across the lifespan. Exercise is an important stimulator of extracellular and intracellular stress signals that promote positive adaptations in skeletal muscle. These adaptations are controlled by changes in gene transcription and protein translation, with many of these molecules identified as potential therapeutic targets to pharmacologically improve muscle quality in patient groups too ill to exercise. MicroRNAs (miRNAs) are recently identified regulators of numerous gene networks and pathways and mainly exert their effect by binding to their target messenger RNAs (mRNAs), resulting in mRNA degradation or preventing protein translation. The role of exercise as a regulatory stimulus of skeletal muscle miRNAs is now starting to be investigated. This review highlights our current understanding of the regulation of skeletal muscle miRNAs with exercise and disease as well as how they may control skeletal muscle health.
Highlights
Maintaining skeletal muscle metabolism, size and contractile function are prerequisites for whole body health throughout life
We demonstrated in vitro, via a reporter assay, that miR-31 directly interacts with HDAC4 (Russell et al, 2013), a component of the MAPK pathway (Symons et al, 2009), as well as with NRF1, which is involved in mitochondrial biogenesis and metabolism
CONCLUDING REMARKS MiRNAs are positive regulators of myogenesis. Their expression levels change following a single bout of exercise and exercise training and following nutritional interventions
Summary
Maintaining skeletal muscle metabolism, size and contractile function are prerequisites for whole body health throughout life. Extracellular and intracellular signals, activated by exercise or disease and inactivity, influence transcriptional and translational regulation of genes encoding proteins that control skeletal muscle metabolism, growth, regeneration and contraction (Dela et al, 1994; Russell et al, 2003, 2005; Short et al, 2003; Wadley et al, 2007). Our understanding of how exercise and disease regulate miRNA expression and activity as well as their messenger RNA (mRNA) targets implicated in skeletal muscle health is rudimentary. The transcriptional regulation of muscle enriched miRNAs is under the control of myogenic regulatory factors (MRFs), such as MyoD, myogenin, Myf and MRF4 (Rao et al, 2006; Rosenberg et al, 2006), that tightly control skeletal muscle regeneration (Rudnicki and Jaenisch, 1995; Tajbakhsh et al, 1996; Sabourin and Rudnicki, 2000) These miRNAs can be arranged in polycistronic clusters and transcribed together or in parallel with protein-coding genes (Sweetman et al, 2008). MiR-206 promotes differentiation of C2C12 myoblasts (Kim et al, 2006) and Frontiers in Physiology | Striated Muscle Physiology
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