| Autor: |
Sharlo KA; Institute of Biomedical Problems, RAS, 123007 Moscow, Russia., Lvova ID; Institute of Biomedical Problems, RAS, 123007 Moscow, Russia., Belova SP; Institute of Biomedical Problems, RAS, 123007 Moscow, Russia., Zaripova KA; Institute of Biomedical Problems, RAS, 123007 Moscow, Russia., Shenkman BS; Institute of Biomedical Problems, RAS, 123007 Moscow, Russia., Nemirovskaya TL; Institute of Biomedical Problems, RAS, 123007 Moscow, Russia. |
| Jazyk: |
angličtina |
| Zdroj: |
International journal of molecular sciences [Int J Mol Sci] 2022 Dec 28; Vol. 24 (1). Date of Electronic Publication: 2022 Dec 28. |
| DOI: |
10.3390/ijms24010503 |
| Abstrakt: |
Muscle unloading leads to signaling alterations that cause muscle atrophy and weakness. The cellular energy sensor AMPK can regulate myofiber-type shift, calcium-dependent signaling and ubiquitin-proteasome system markers. We hypothesized that the prevention of p-AMPK downregulation during the first week of muscle unloading would impede atrophy development and the slow-to-fast shift of soleus muscle fibers, and the aim of the study was to test this hypothesis. Thirty-two male Wistar rats were randomly assigned to four groups: placebo control (C), control rats treated with metformin (C + M), 7 days of hindlimb suspension (HS) + placebo (7HS), and 7 days of HS + metformin administration (7HS + M). In the soleus of the 7HS rats, we detected a slow-to-fast fiber-type shift as well as a significant downregulation of MEF-2D and p300 in the nuclei. In the 7HS group, we also found decreases in p-ACC (AMPK target) protein level and in the expression of E3 ubiquitin ligases and p-CaMK II protein level vs. the C group. The 7-day metformin treatment for soleus muscle unloading (1) prevented slow-to-fast fiber-type shift; (2) counteracted changes in the p-ACC protein level; (3) hindered changes in the nuclear protein level of the slow myosin expression activators MEF-2D and p300, but did not affect NFATc1 signaling; and (4) attenuated the unloading-induced upregulation of MuRF-1, atrogin-1, ubiquitin and myostatin mRNA expression, but did not prevent soleus muscle atrophy. Thus, metformin treatment during muscle disuse could be useful to prevent the decrease in the percentage of slow-type fatigue-resistant muscle fibers. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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