scholarly journals Tibial Nerve Transection - A Standardized Model for Denervation-induced Skeletal Muscle Atrophy in Mice

Author(s):  
Jane A. E. Batt ◽  
James Ralph Bain
2019 ◽  
Vol 316 (3) ◽  
pp. C456-C461 ◽  
Author(s):  
Haiming Liu ◽  
LaDora V. Thompson

Unilateral denervation is widely used for studies investigating mechanisms of muscle atrophy. The “contralateral-innervated muscle” is a commonly used experimental control in denervation studies. It is not clear whether denervation unilaterally alters the proteolytic system in the contralateral-innervated muscles. Therefore, the objectives of this rapid report are 1) to determine whether unilateral denervation has an effect on the proteolytic system in contralateral-innervated control muscles and 2) to identify the changes in proteasome properties in denervated muscles after 7- and 14-day tibial nerve transection with either the contralateral-innervated muscles or intact muscles from nonsurgical mice used as the experimental control. In the contralateral-innervated muscles after 7 and 14 days of nerve transection, the proteasome activities and content are significantly increased compared with muscles from nonsurgical mice. When the nonsurgical mice are used as the experimental control, a robust increase in proteasome properties is found in the denervated muscles. This robust increase in proteasome properties is eliminated when the contralateral-innervated muscles are the experimental control. In conclusion, there is a crossover effect from unilateral denervation on proteolytic parameters. As a result, the crossover effect on contralateral-innervated muscles must be considered when an experimental control is selected in a denervation study.


2019 ◽  
Vol 6 (1) ◽  
Author(s):  
Jeffrey T. Ehmsen ◽  
Riki Kawaguchi ◽  
Ruifa Mi ◽  
Giovanni Coppola ◽  
Ahmet Höke

Abstract Skeletal muscle is a highly adaptable tissue capable of changes in size, contractility, and metabolism according to functional demands. Atrophy is a decline in mass and strength caused by pathologic loss of myofibrillar proteins, and can result from disuse, aging, or denervation caused by injury or peripheral nerve disorders. We provide a high-quality longitudinal RNA-Seq dataset of skeletal muscle from a cohort of adult C57BL/6J male mice subjected to tibial nerve denervation for 0 (baseline), 1, 3, 7, 14, 30, or 90 days. Using an unbiased genomics approach to identify gene expression changes across the entire longitudinal course of muscle atrophy affords the opportunity to (1) establish acute responses to denervation, (2) detect pathways that mediate rapid loss of muscle mass within the first week after denervation, and (3) capture the molecular phenotype of chronically atrophied muscle at a stage when it is largely resistant to recovery.


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