Modelling Skeletal Muscle Ageing and Repair In Vitro

Author:

Tarum Janelle1ORCID,Degens Hans23ORCID,Turner Mark D.4ORCID,Stewart Claire5ORCID,Sale Craig6ORCID,Santos Lívia1ORCID

Affiliation:

1. Department of Sport Science, Sport Health and Performance Enhancement Research Centre (SHAPE), School of Science and Technology, Nottingham Trent University, Nottingham, UK

2. Musculoskeletal Science and Sports Medicine Research Centre, Department of Life Sciences, Manchester Metropolitan University Institute of Sport, Manchester Metropolitan University, Manchester, UK

3. Lithuanian Sports University, Kaunas, Lithuania

4. Centre for Diabetes, Chronic Diseases and Ageing, School of Science and Technology, Nottingham Trent University, Clifton, UK

5. Research Institute of Sport and Exercise Science, Liverpool John Moores University, Liverpool, UK

6. Institute of Sport, Manchester Metropolitan University, Manchester, UK

Abstract

Healthy skeletal muscle can regenerate after ischaemic, mechanical, or toxin-induced injury, but ageing impairs that regeneration potential. This has been largely attributed to dysfunctional satellite cells and reduced myogenic capacity. Understanding which signalling pathways are associated with reduced myogenesis and impaired muscle regeneration can provide valuable information about the mechanisms driving muscle ageing and prompt the development of new therapies. To investigate this, we developed a high-throughput in vitro model to assess muscle regeneration in chemically injured C2C12 and human myotube-derived young and aged myoblast cultures. We observed a reduced regeneration capacity of aged cells, as indicated by an attenuated recovery towards preinjury myotube size and myogenic fusion index at the end of the regeneration period, in comparison with younger muscle cells that were fully recovered. RNA-sequencing data showed significant enrichment of KEGG signalling pathways, PI3K-Akt, and downregulation of GO processes associated with muscle development, differentiation, and contraction in aged but not in young muscle cells. Data presented here suggest that repair in response to in vitro injury is impaired in aged vs. young muscle cells. Our study establishes a framework that enables further understanding of the factors underlying impaired muscle regeneration in older age.

Funder

Marie Skłodowska-Curie DTA COFUND

Publisher

Hindawi Limited

Subject

Biomedical Engineering,Biomaterials,Medicine (miscellaneous)

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