Effect of resistance training on satellite cells in old mice – a transcriptome study

Author:

Hsu Wei-Bin1ORCID,Lin Shih-Jie23ORCID,Hung Ji-Shiuan4ORCID,Chen Mei-Hsin45ORCID,Lin Che-Yi6ORCID,Hsu Wei-Hsiu45ORCID,Hsu Wen-Wei Robert145ORCID

Affiliation:

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

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.

Publisher

British Editorial Society of Bone & Joint Surgery

Subject

Orthopedics and Sports Medicine,Surgery

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