Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/4249
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Title: The effects of low frequency electrical stimulation on satellite cell activity in rat skeletal muscle during hindlimb suspension
Authors: Zhang, BT
Yeung, SMS 
Liu, Y
Wang, HH
Wan, YM
Ling, SK
Zhang, HY
Li, YH
Yeung, WE 
Issue Date: 2010
Source: BMC cell biology, 2010, v. 11, 87, p. 1-9
Abstract: Background: The ability of skeletal muscle to grow and regenerate is dependent on resident stem cells called satellite cells. It has been shown that chronic hindlimb unloading downregulates the satellite cell activity. This study investigated the role of low-frequency electrical stimulation on satellite cell activity during a 28 d hindlimb suspension in rats.
Results: Mechanical unloading resulted in a 44% reduction in the myofiber cross-sectional area as well as a 29% and 34% reduction in the number of myonuclei and myonuclear domains, respectively, in the soleus muscles (P < 0.001 vs the weight-bearing control). The number of quiescent (M-cadherin[sup +]), proliferating (BrdU[sup +] and myoD[sup +]), and differentiated (myogenin[sup +]) satellite cells was also reduced by 48-57% compared to the weight-bearing animals (P < 0.01 for all). Daily application of electrical stimulation (2 × 3 h at a 20 Hz frequency) partially attenuated the reduction of the fiber cross-sectional area, satellite cell activity, and myonuclear domain (P < 0.05 for all). Extensor digitorum longus muscles were not significantly altered by hindlimb unloading.
Conclusion: This study shows that electrical stimulation partially attenuated the decrease in muscle size and satellite cells during hindlimb unloading. The causal relationship between satellite cell activation and electrical stimulation remain to be established.
Publisher: BioMed Central
Journal: BMC cell biology 
EISSN: 1471-2121
DOI: 10.1186/1471-2121-11-87
Rights: © 2010 Zhang et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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