ABSTRACT
The clinical treatment of joint contracture due to immobilization remains difficult. The pathological changes of muscle tissue caused by immobilization-induced joint contracture include disuse skeletal muscle atrophy and skeletal muscle tissue fibrosis. The proteolytic pathways involved in disuse muscle atrophy include the ubiquitin-proteasome-dependent pathway, caspase system pathway, matrix metalloproteinase pathway, Ca-dependent pathway and autophagy-lysosomal pathway. The important biological processes involved in skeletal muscle fibrosis include intermuscular connective tissue thickening caused by transforming growth factor-β1 and an anaerobic environment within the skeletal muscle leading to the induction of hypoxia-inducible factor-1α. This article reviews the progress made in understanding the pathological processes involved in immobilization-induced muscle contracture and the currently available treatments. Understanding the mechanisms involved in immobilization-induced contracture of muscle tissue should facilitate the development of more effective treatment measures for the different mechanisms in the future.
Subject(s)
Humans , Atrophy , Autophagy , Calcium , Metabolism , Caspases , Metabolism , Connective Tissue , Metabolism , Pathology , Contracture , Metabolism , Pathology , Therapeutics , Fibrosis , Immobilization , Joints , Lysosomes , Metabolism , Matrix Metalloproteinases , Metabolism , Muscle, Skeletal , Metabolism , Pathology , Proteasome Endopeptidase Complex , Metabolism , Proteolysis , Signal Transduction , Physiology , Transforming Growth Factor beta1 , Metabolism , Ubiquitin , MetabolismABSTRACT
Electroacupuncture (EA) is an acupuncture technique that is stimulated by acupuncture needles with low-frequency microcurrent. The aim of this study is to elucidate the effect of EA and it's molecular mechanism on muscle atrophy by using an animal model: hindlimb-suspended (HS) mice in the disuse muscle atrophy model. To compare the effects of EA in HS mice and HS mice treated with EA (EA/HS), soleus muscle mass and soleus myofiber diameter were measured. We then used real-time quantitative RT-PCR to analyze the expression of myostatin and ubiquitin ligase genes in atrophic muscles of HS mice and in muscles of EA/HS mice. We found that EA/HS mice maintained a soleus muscle mass that was not significantly different from that of wild mice (WT), whereas HS mice had significantly reduced muscle mass. Also, the diameters of myofibers in EA/HS mice, which were not significantly different from wild values, were significantly larger than those in HS mice. Repeated EA treatment suppressed gene expression of myostatin and ubiquitin ligase genes in skeletal muscle of EA/HS mice but induced expression of these genes in HS mice. These findings suggest the molecular mechanism by EA: suppression of myostatin and ubiquitin ligase gene may be a key reaction of inhibiting the disuse muscle atrophy.
ABSTRACT
Electroacupuncture (EA) is an acupuncture technique that is stimulated by acupuncture needles with low-frequency microcurrent. The aim of this study is to elucidate the effect of EA and it's molecular mechanism on muscle atrophy by using an animal model: hindlimb-suspended (HS) mice in the disuse muscle atrophy model. To compare the effects of EA in HS mice and HS mice treated with EA (EA/HS), soleus muscle mass and soleus myofiber diameter were measured. We then used real-time quantitative RT-PCR to analyze the expression of myostatin and ubiquitin ligase genes in atrophic muscles of HS mice and in muscles of EA/HS mice. We found that EA/HS mice maintained a soleus muscle mass that was not significantly different from that of wild mice (WT), whereas HS mice had significantly reduced muscle mass. Also, the diameters of myofibers in EA/HS mice, which were not significantly different from wild values, were significantly larger than those in HS mice. Repeated EA treatment suppressed gene expression of myostatin and ubiquitin ligase genes in skeletal muscle of EA/HS mice but induced expression of these genes in HS mice. These findings suggest the molecular mechanism by EA: suppression of myostatin and ubiquitin ligase gene may be a key reaction of inhibiting the disuse muscle atrophy.