Abstract:
AIM:Muscle atrophy is a common symptom after nerve denervation. Myostatin propeptide, a precursor of myostatin, has been documented to improve muscle growth. However, the mechanism underlying the muscle atrophy attenuation effects of myostatin propeptide in muscles and the changes in gene expression are not well established. We investigated the possible underlying mechanisms associated with myostatin propeptide gene delivery by gene gun in a rat denervation muscle atrophy model, and evaluated gene expression patterns. MAIN METHODS:In a rat botulinum toxin-induced nerve denervation muscle atrophy model, we evaluated the effects of wild-type (MSPP) and mutant-type (MSPPD75A) of myostatin propeptide gene delivery, and observed changes in gene activation associated with the neuromuscular junction, muscle and nerve. KEY FINDINGS:Muscle mass and muscle fiber size was moderately increased in myostatin propeptide treated muscles (p<0.05). And enhancement of the gene expression of the muscle regulatory factors, neurite outgrowth factors (IGF-1, GAP43) and acetylcholine receptors was observed. Our results demonstrate that myostatin propeptide gene delivery, especially the mutant-type of MSPPD75A, attenuates muscle atrophy through myogenic regulatory factors and acetylcholine receptor regulation. SIGNIFICANCE:Our data concluded that myostatin propeptide gene therapy may be a promising treatment for nerve denervation induced muscle atrophy.
journal_name
Life Scijournal_title
Life sciencesauthors
Tsai SW,Tung YT,Chen HL,Yang SH,Liu CY,Lu M,Pai HJ,Lin CC,Chen CMdoi
10.1016/j.lfs.2015.12.056subject
Has Abstractpub_date
2016-02-01 00:00:00pages
15-23eissn
0024-3205issn
1879-0631pii
S0024-3205(15)30147-8journal_volume
146pub_type
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