BMC Medical Genomics (Mar 2024)

Swimming exercise reverses transcriptomic changes in aging mouse lens

  • Lin Ye,
  • Jiayue Yuan,
  • Shijie Zhu,
  • Shunmei Ji,
  • Jinhui Dai

DOI
https://doi.org/10.1186/s12920-024-01839-1
Journal volume & issue
Vol. 17, no. 1
pp. 1 – 11

Abstract

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Abstract Background The benefits of physical activity for the overall well-being of elderly individuals are well-established, the precise mechanisms through which exercise improves pathological changes in the aging lens have yet to be fully understood. Methods 3-month-old C57BL/6J mice comprised young sedentary (YS) group, while aging mice (18-month-old) were divided into aging sedentary (AS) group and aging exercising (AE) group. Mice in AE groups underwent sequential stages of swimming exercise. H&E staining was employed to observe alterations in lens morphology. RNA-seq analysis was utilized to examine transcriptomic changes. Furthermore, qPCR and immunohistochemistry were employed for validation of the results. Results AE group showed alleviation of histopathological aging changes in AS group. By GSEA analysis of the transcriptomic changes, swimming exercise significantly downregulated approximately half of the pathways that underwent alterations upon aging, where notable improvements were ‘calcium signaling pathway’, ‘neuroactive ligand receptor interaction’ and ‘cell adhesion molecules’. Furthermore, we revealed a total of 92 differentially expressed genes between the YS and AS groups, of which 10 genes were observed to be mitigated by swimming exercise. The result of qPCR was in consistent with the transcriptome data. We conducted immunohistochemical analysis on Ciart, which was of particular interest due to its dual association as a common aging gene and its significant responsiveness to exercise. The Protein-protein Interaction network of Ciart showed the involvement of the regulation of Rorb and Sptbn5 during the process. Conclusion The known benefits of exercise could extend to the aging lens and support further investigation into the specific roles of Ciart-related pathways in aging lens.

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