Long-Term Exercise Protects against Cellular Stresses in Aged Mice
Autor: | Irina Belaya; Masataka Suwa; Tao Chen; Rashid Giniatullin; Katja M. Kanninen; Mustafa Atalay; Shuzo Kumagai |
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Sprache: | Englisch |
Veröffentlicht: |
2018 |
Quelle: | Directory of Open Access Journals: DOAJ Articles |
Online Zugang: |
http://dx.doi.org/10.1155/2018/2894247 https://doaj.org/toc/1942-0900 https://doaj.org/toc/1942-0994 1942-0900 1942-0994 doi:10.1155/2018/2894247 https://doaj.org/article/10f0d21d89a94e2cbcb61453809bd650 https://doi.org/10.1155/2018/2894247 https://doaj.org/article/10f0d21d89a94e2cbcb61453809bd650 |
Erfassungsnummer: | ftdoajarticles:oai:doaj.org/article:10f0d21d89a94e2cbcb61453809bd650 |
Zusammenfassung
The current study examined the effect of aging and long-term wheel-running on the expression of heat shock protein (HSP), redox regulation, and endoplasmic reticulum (ER) stress markers in tibialis anterior (T.A.) and soleus muscle of mice. Male mice were divided into young (Y, 3-month-old), old-sedentary (OS, 24-month-old), and old-exercise (OE, 24-month-old) groups. The OE group started voluntary wheel-running at 3 months and continued until 24 months of age. Aging was associated with a higher thioredoxin-interacting protein (TxNiP) level, lower thioredoxin-1 (TRX-1) to TxNiP ratio—a determinant of redox regulation and increased CHOP, an indicator of ER stress-related apoptosis signaling in both muscles. Notably, GRP78, a key indicator of ER stress, was selectively elevated in T.A. Long-term exercise decreased TxNiP in T.A. and soleus muscles and increased the TRX-1/TxNiP ratio in soleus muscle of aged mice. Inducible HSP70 and constituent HSC70 were upregulated, whereas CHOP was reduced after exercise in soleus muscle. Thus, our data demonstrated that aging induced oxidative stress and activated ER stress-related apoptosis signaling in skeletal muscle, whereas long-term wheel-running improved redox regulation, ER stress adaptation and attenuated ER stress-related apoptosis signaling. These findings suggest that life-long exercise can protect against age-related cellular stress.