Volume 22, Issue 1 (4-2019)
J Arak Uni Med Sci 2019, 22(1): 51-61 |
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Hadidi V, Daryanoosh F, Nemati J, Tanideh N. The Effect of Hind Limb Immobilization on Expression of Some Genes Involved in the Regulation of Mitochondrial Processes in Soleus Muscle of Trained and Untrained Rats. J Arak Uni Med Sci 2019; 22 (1) :51-61
URL: http://jams.arakmu.ac.ir/article-1-5866-en.html
URL: http://jams.arakmu.ac.ir/article-1-5866-en.html
1- Department of Exercise Physiology, Faculty of Psychology and Educational Science, Shiraz University, Shiraz, Iran.
2- Department of Exercise Physiology, Faculty of Psychology and Educational Science, Shiraz University, Shiraz, Iran. , daryanoosh@shirazu.ac.ir
3- Stem Cell Technology Research Center, Department of Pharmacology, Shiraz University of Medicine Science, Shiraz, Iran.
2- Department of Exercise Physiology, Faculty of Psychology and Educational Science, Shiraz University, Shiraz, Iran. , daryanoosh@shirazu.ac.ir
3- Stem Cell Technology Research Center, Department of Pharmacology, Shiraz University of Medicine Science, Shiraz, Iran.
Abstract: (2571 Views)
Background and Aim: The purpose of this study was to determine the effect of a hind limb immobilization on the expression of PGC-1α, NRF1, Mfn2, PINK1 and Drp1 genes as the main regulators of mitochondrial quality and function in soleus muscle of endurance trained rats.
Materials and Methods: In this study, 15 male Sprague-Dawley rats were divided into three groups (control, exercise +immobilization and immobilization). The exercise + immobilization group run on the treadmill for 12 weeks and five times per week. The hind limb of the animal was immobilized for seven days with the casting method. Soleus muscle was extracted and the expression of the genes was measured by RT-PCR method. Univariate ANOVA and Tukey post hoc test were used to determine the differences (α = 0.05).
Ethical Considerations: This study with research ethics code IR.SUMS.REC.1396.S444 has been approved by research ethics committee at Shiraz university of medical sciences, Iran.
Findings: Results showed that immobilization in both immobilization and exercise +immobilization groups, compared to the conterl group, reduced the expression of PGC-1α gene (p = 0.001 and p = 0.045), NRF1 (p = 0.001 and p = 0.006), Mfn2 (p = 0.001, p = 0.001) and increased the expression of PINK1 (p = 0.001 and p= 0.001), but the expression of Drp1 gene didn't change significantly (p = 0.069 and p = 0.223). Also, studies showed that the expression of PGC-1α (p = 0.013), NRF1 (p = 0.001) and Mfn2 (p = 0.001) in the exercise + immobilization was lower in compare with the immobilization group. The expression of PINK1 was lower than immobilization group as well (p = 0.001).
Conclusion: This study shows that endurance training has a protective effect on mitochondrial quality during the immobilization period, but it can't prevent mitochondrial dysfunction.
Materials and Methods: In this study, 15 male Sprague-Dawley rats were divided into three groups (control, exercise +immobilization and immobilization). The exercise + immobilization group run on the treadmill for 12 weeks and five times per week. The hind limb of the animal was immobilized for seven days with the casting method. Soleus muscle was extracted and the expression of the genes was measured by RT-PCR method. Univariate ANOVA and Tukey post hoc test were used to determine the differences (α = 0.05).
Ethical Considerations: This study with research ethics code IR.SUMS.REC.1396.S444 has been approved by research ethics committee at Shiraz university of medical sciences, Iran.
Findings: Results showed that immobilization in both immobilization and exercise +immobilization groups, compared to the conterl group, reduced the expression of PGC-1α gene (p = 0.001 and p = 0.045), NRF1 (p = 0.001 and p = 0.006), Mfn2 (p = 0.001, p = 0.001) and increased the expression of PINK1 (p = 0.001 and p= 0.001), but the expression of Drp1 gene didn't change significantly (p = 0.069 and p = 0.223). Also, studies showed that the expression of PGC-1α (p = 0.013), NRF1 (p = 0.001) and Mfn2 (p = 0.001) in the exercise + immobilization was lower in compare with the immobilization group. The expression of PINK1 was lower than immobilization group as well (p = 0.001).
Conclusion: This study shows that endurance training has a protective effect on mitochondrial quality during the immobilization period, but it can't prevent mitochondrial dysfunction.
References
1. Weinberg F, Hamanaka R, Wheaton WW, Weinberg S, Joseph J, Lopez M, et al. Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity. Proceedings of the National Academy of Sciences. 2010; 107(19):8788-93.
2. Kuznetsov AV, Margreiter R. Heterogeneity of mitochondria and mitochondrial function within cells as another level of mitochondrial complexity. International journal of molecular sciences. 2009; 10(4):1911-29.
3. Twig G, Shirihai OS. The interplay between mitochondrial dynamics and mitophagy. Antioxidants & redox signaling. 2011; 14(10):1939-51.
4. Rojo M, Legros F, Chateau D, Lombès A. Membrane topology and mitochondrial targeting of mitofusins, ubiquitous mammalian homologs of the transmembrane GTPase Fzo. Journal of cell science. 2002; 115(8):1663-74.
5. Narendra D, Tanaka A, Suen DF, Youle RJ. Parkin is recruited selectively to impaired mitochondria and promotes their autophagy. The Journal of cell biology. 2008; 183(5):795-803.
6. Adhihetty PJ, Uguccioni G, Leick L, Hidalgo J, Pilegaard H, Hood DA. The role of PGC-1α on mitochondrial function and apoptotic susceptibility in muscle. American Journal of Physiology-Cell Physiology. 2009; 297(1):C217-25.
7. Santel A, Fuller MT. Control of mitochondrial morphology by a human mitofusin. Journal of cell science. 2001; 114(5):867-74.
8. Ishihara N, Eura Y, Mihara K. Mitofusin 1 and 2 play distinct roles in mitochondrial fusion reactions via GTPase activity. Journal of cell science. 2004; 117(26):6535-46.
9. Sandri M, Lin J, Handschin C, Yang W, Arany ZP, Lecker SH, et al. PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription. Proceedings of the National Academy of Sciences. 2006; 103(44):16260-5.
10. Adhihetty PJ, O'Leary MF, Chabi B, Wicks KL, Hood DA. Effect of denervation on mitochondrially mediated apoptosis in skeletal muscle. Journal of applied physiology. 2007; 102(3):1143-51.
11. Iqbal S, Ostojic O, Singh K, Joseph AM, Hood DA. Expression of mitochondrial fission and fusion regulatory proteins in skeletal muscle during chronic use and disuse. Muscle & nerve. 2013; 48(6):963-70.
12. Wagatsuma A, Kotake N, Mabuchi K, Yamada S. Expression of nuclear-encoded genes involved in mitochondrial biogenesis and dynamics in experimentally denervated muscle. Journal of physiology and biochemistry. 2011; 7(3):359-70.
13. Aoi W, Naito Y, Mizushima K, Takanami Y, Kawai Y, Ichikawa H, et al. The microRNA miR-696 regulates PGC-1α in mouse skeletal muscle in response to physical activity. American Journal of Physiology-Endocrinology and Metabolism. 2010; 298(4):E799-806.
14. Frimel TN, Kapadia F, Gaidosh GS, Li Y, Walter GA, Vandenborne K. A model of muscle atrophy using cast immobilization in mice. Muscle & nerve. 2005; 32(5):672-4.
15. Kang C, Chung E, Diffee G, Ji LL. Exercise training attenuates aging-associated mitochondrial dysfunction in rat skeletal muscle: role of PGC-1α. Experimental gerontology. 2013; 48(11):1343-50.
16. Wicks KL, Hood DA. Mitochondrial adaptations in denervated muscle: relationship to muscle performance. American Journal of Physiology-Cell Physiology. 1991; 260(4):C841-50.
17. Mittler R. Oxidative stress, antioxidants and stress tolerance. Trends in plant science. 2002; 7(9):405-10.
18. Youn JY, Zhang J, Zhang Y, Chen H, Liu D, Ping P, et al. Oxidative stress in atrial fibrillation: an emerging role of NADPH oxidase. Journal of molecular and cellular cardiology. 2013; 62:72-9.
19. Ono T, Isobe K, Nakada K, Hayashi JI. Human cells are protected from mitochondrial dysfunction by complementation of DNA products in fused mitochondria. Nature genetics. 2001; 28(3):272-5.
20. Bach, D., Pich, S., Soriano, F. X., Vega, N., Baumgartner, B., Oriola, J., ... et al. Mitofusin-2 determines mitochondrial network architecture and mitochondrial metabolism A novel regulatory mechanism altered in obesity. Journal of Biological Chemistry. 2003; 278(19): 17190-17197.
21. Sacheck, J. M., Hyatt, J. P. K., Raffaello, A., Jagoe, R. T., Roy, R. R., Edgerton, V. R., ... et al .Rapid disuse and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases. The FASEB Journal. 2007; 21 (1), 140-155.
22. Bartlett SR, Sawdy R, Mann GE. Induction of cyclooxygenase‐2 expression in human myometrial smooth muscle cells by interleukin‐1β: involvement of p38 mitogen‐activated protein kinase. The Journal of physiology. 1999; 520(2):399-406.
23. Kang C, Goodman CA, Hornberger TA, Ji LL. PGC-1α overexpression by in vivo transfection attenuates mitochondrial deterioration of skeletal muscle caused by immobilization. The FASEB Journal. 2015; 29(10):4092-106.
24. Faist V, König J, Höger H, Elmadfa I. Decreased mitochondrial oxygen consumption and antioxidant enzyme activities in skeletal muscle of dystrophic mice after low-intensity exercise. Annals of nutrition and metabolism. 2001; 45(2):58-66.
25. Langfort J, Viese M, Ploug T, Dela F. Time course of GLUT4 and AMPK protein expression in human skeletal muscle during one month of physical training. Scandinavian journal of medicine & science in sports. 2003; 13(3):169-74.
26. Phillips SM, Green HJ, Tarnopolsky MA, Heigenhauser GJ, Grant SM. Progressive effect of endurance training on metabolic adaptations in working skeletal muscle. American Journal of Physiology-Endocrinology And Metabolism. 1996; 270(2):E265-72.
27. Hadidi V, Kordi M, Gaeini A, Nekoie A, Shafie A, Hajati Modaraie M. Effect of eight weeks high intensity interval training on gene expression of PGC-1α, in male healthy rats fast-slow twitch muscles. Harkat journal. 2015; 7(4): 661-673. (In Persian).
28. Powers SK, Wiggs MP, Duarte JA, Zergeroglu AM, Demirel HA. Mitochondrial signaling contributes to disuse muscle atrophy. American Journal of Physiology-Endocrinology and Metabolism. 2012 .
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