Effect of resistance training on satellite cells in old mice - a transcriptome study : implications for sarcopenia

Wei-Bin Hsu; Shih-Jie Lin; Ji-Shiuan Hung; Mei-Hsin Chen; Che-Yi Lin; Wei-Hsiu Hsu; Wen-Wei Robert Hsu

doi:10.1302/2046-3758.112.BJR-2021-0079.R2

Effect of resistance training on satellite cells in old mice - a transcriptome study : implications for sarcopenia

Bone Joint Res. 2022 Feb;11(2):121-133. doi: 10.1302/2046-3758.112.BJR-2021-0079.R2.

Authors

Wei-Bin Hsu¹, Shih-Jie Lin^{2

3}, Ji-Shiuan Hung⁴, Mei-Hsin Chen^{4

5}, Che-Yi Lin⁶, Wei-Hsiu Hsu^{4

5}, Wen-Wei Robert Hsu^{1

4

5}

Affiliations

¹ Sports Medicine Center, Chang Gung Memorial Hospital Chiayi Branch, Puzi, Taiwan.
² Department of Orthopaedic Surgery, New Taipei City Municipal Tucheng Hospital, New Taipei City, Taiwan.
³ Bone and Joint Research Center, Chang Gung Memorial Hospital, Linkou, Taiwan.
⁴ Department of Orthopaedic Surgery, Chang Gung Memorial Hospital Chiayi Branch, Chiayi, Taiwan.
⁵ Chang Gung University, Taoyuan, Taiwan.
⁶ Institute of Cellular and Organismic Biology Academia Sinica, Taipei, Taiwan.

PMID: 35188421
PMCID: PMC8882320
DOI: 10.1302/2046-3758.112.BJR-2021-0079.R2

Abstract

Aims: The decrease in the number of satellite cells (SCs), contributing to myofibre formation and reconstitution, and their proliferative capacity, leads to muscle loss, a condition known as sarcopenia. Resistance training can prevent muscle loss; however, the underlying mechanisms of resistance training effects on SCs are not well understood. We therefore conducted a comprehensive transcriptome analysis of SCs in a mouse model.

Methods: We compared the differentially expressed genes of SCs in young mice (eight weeks old), middle-aged (48-week-old) mice with resistance training intervention (MID+ T), and mice without exercise (MID) using next-generation sequencing and bioinformatics.

Results: After the bioinformatic analysis, the PI3K-Akt signalling pathway and the regulation of actin cytoskeleton in particular were highlighted among the top ten pathways with the most differentially expressed genes involved in the young/MID and MID+ T/MID groups. The expression of Gng5, Atf2, and Rtor in the PI3K-Akt signalling pathway was higher in the young and MID+ T groups compared with the MID group. Similarly, Limk1, Arhgef12, and Araf in the regulation of the actin cytoskeleton pathway had a similar bias. Moreover, the protein expression profiles of Atf2, Rptor, and Ccnd3 in each group were paralleled with the results of NGS.

Conclusion: Our results revealed that age-induced muscle loss might result from age-influenced genes that contribute to muscle development in SCs. After resistance training, age-impaired genes were reactivated, and age-induced genes were depressed. The change fold in these genes in the young/MID mice resembled those in the MID + T/MID group, suggesting that resistance training can rejuvenate the self-renewing ability of SCs by recovering age-influenced genes to prevent sarcopenia. Cite this article: Bone Joint Res 2022;11(2):121-133.

Keywords: Age-induced sarcopenia; RNA; Resistance training; Satellite cells; actin; antibodies; cancer; grip strength; mouse model; muscle fibre; muscle strength loss; resistance training; western blotting.