Research ArticleOpen AccessGoogle Scholar indexed
Overexpression of MyoD Attenuates Denervated Rat Skeletal Muscle Atrophy and Dysfunction
Department of Gastroenterology, Shanghai 445 Hospital, Shanghai, China
Medical College of Shanghai Jiao Tong University, Shanghai, China.
Medical College of Shanghai Jiao Tong University, Shanghai, China.
Medical College of Shanghai Jiao Tong University, Shanghai, China.
Medical College of Shanghai Jiao Tong University, Shanghai, China.
Medical College of Shanghai Jiao Tong University, Shanghai, China.
Medical College of Shanghai Jiao Tong University, Shanghai, China.
- 1 Department of Gastroenterology, Shanghai 445 Hospital, Shanghai, China
- 2 Medical College of Shanghai Jiao Tong University, Shanghai, China.
- 3 Medical College of Shanghai Jiao Tong University, Shanghai, China.
- 4 Medical College of Shanghai Jiao Tong University, Shanghai, China.
- 5 Medical College of Shanghai Jiao Tong University, Shanghai, China.
- 6 Medical College of Shanghai Jiao Tong University, Shanghai, China.
- 7 Medical College of Shanghai Jiao Tong University, Shanghai, China.
Neuroscience and Medicine·Volume 03 (2012)·Pages 387–393·Published 21 December 2012·DOI10.4236/nm.2012.34048
Copy link · social · email
Abstract
Nerve injury commonly contributes to irreversible functional impairment, reconstruction of the function of muscle is big challenge. In denervated skeletal muscle, therapid expression of MyoD mRNA and protein also occurs during early postdenervation, which suggested that the function of denervation-induced MyoD may be to prevent denervation-induced skeletal muscle atrophy. However, the detail mechanism is not clear. Therefore, in this study, we established a stable-transfected MyoD L6 cell line. After the operation for cutting the rats’ tibial nerve, the MyoD-L6 cells were injected in the gastrocnemius, the function of the gastronemius was monitored. It was found that injected the MyoD-L6 cells could attenuate the muscle atrophy and dysfunction. Therefore, overexpression of MyoD could serve as a new therapy strategy to cure denervation-induced dysfunction of skeletal muscle.
KeywordsMyoDDenervationRat Skeletal MuscleAtrophyDysfunction
- P. J. Plant, J. R. Bain, J. E. Correa, M. Woo and J. Batt, “Absence of Caspase-3 Protects Against Denervation-Induced Skeletal Muscle Atrophy,” Journal of Applied Physiology, Vol. 107, No. 1, 2009, pp. 224-234. doi:10.1152/japplphysiol.90932.2008
- P. M. Siu and S. E. Always, “Response and Adaptation of Skeletal Muscle to Denervation Stress: The Role of Apoptosis in Muscle Loss,” Frontiers in Bioscience, Vol. 14, 2009, pp. 432-452. doi:10.2741/3253
- B. C. Beehler, P. G. Sleph, L. Benmassaoud and G. J. Grover, “Reduction of Skeletal Muscle Atrophy by a Proteasome Inhibitor in a Rat Model of Denervation,” Experimental Biology and Medicine (Maywood), Vol. 231, No. 3, 2006, pp. 335-341.
- F. L. Muller, W. Song, et al., “Denervation-Induced Skeletal Muscle Atrophy is Associated with Increased Mitochondrial ROS Production,” American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Vol. 293, No. 3, 2007, pp. R1159-R1168. doi:10.1152/ajpregu.00767.2006
- S. L. Rowan, K. Rygiel, F. M. Purves-Smith, N. M. Solbak, D. M. Turnbull and R. T. Hepple, “Denervation Causes Fiber Atrophy and Myosin Heavy Chain Co-Expression in Senescent Skeletal Muscle,” PLoS One, Vol. 7, No. 1, 2012, p. e29082. doi:10.1371/journal.pone.0029082
- T. Shavlakadze, J. D. White, M. Davies, J. F. Hoh and M. D. Grounds, “Insulin-Like Growth Factor I Slows the Rate of Denervation Induced Skeletal Muscle Atrophy,” Neuromuscular Disorders, Vol. 15, No. 2, 2005, pp. 139-146. doi:10.1016/j.nmd.2004.10.013
- M. Ishido, K. Kami and M. Masuhara, “In Vivo Expression Patterns of MyoD, P21, and Rb Proteins In myonuclei and Satellite Cells of Denervated Rat Skeletal Muscle,” American Journal of Physiology: Cell Physiology, Vol. 287, No. 2, 2004, pp. C484-C493. doi:10.1152/ajpcell.00080.2004
- A. Buonanno, L. Apone, M. I. Morasso, R. Beers, H. R. Brenner and R. Eftimie, “The MyoD Family of Myogenic Factors is Regulated by Electrical Activity: Isolation and Characterization of a Mouse Myf-5 CDNA,” Nucleic Acids Research, Vol. 20, No. 3, 1992, pp. 539-544. doi:10.1093/nar/20.3.539
- J. P. Hyatt, R. R. Roy, K. M. Baldwin and V. R. Edgerton, “Nerve Activity-Independent Regulation of Skeletal Muscle Atrophy: Role of MyoD and Myogenin in Satellite Cells and Myonuclei,” American Journal of Physiology: Cell Physiology, Vol. 285, No. 5, 2003, pp. C1161-C1173.
- K. Koishi, M. Zhang, I. S. McLennan and A. J. Harris, “MyoD Protein Accumulates in Satellite Cells and Is Neurally Regulated in Regenerating Myotubes and Skeletal Muscle Fibers,” Developmental Dynamics, Vol. 202, No. 3, 1995, pp. 244-254. doi:10.1002/aja.1002020304