. Osteoactivin upregulates expression of MMP-3 and MMP-9 in fibroblasts infiltrated into denervated skeletal muscle in mice. Am J Physiol Cell Physiol 289: C697-C707, 2005; doi:10.1152/ajpcell.00565.2004.-In this study, we examined pathophysiological roles of osteoactivin, a functionally unknown type I membrane glycoprotein, in mouse skeletal muscle atrophied by denervation (sciatic neurectomy). Denervation increased the amounts of osteoactivin, vimentin, matrix metalloproteinase-3 (MMP-3), and MMP-9 in mouse gastrocnemius muscle. Interestingly, immunohistochemical analysis revealed that vimentin, MMP-3, and MMP-9 were mainly present in fibroblast-like cells infiltrated into denervated mouse gastrocnemius muscle, whereas osteoactivin was expressed in the sarcolemma of myofibers adjacent to the fibroblast-like cells. On the basis of these findings, we reasoned that osteoactivin in myocytes was involved in activation of the infiltrated fibroblasts. To address this issue, we examined effects of osteoactivin on expression of MMPs in fibroblasts in vitro and in vivo. Overexpression of osteoactivin in NIH-3T3 fibroblasts induced expression of MMP-3, but not in mouse C 2C12 myoblasts, indicating that osteoactivin might functionally target fibroblasts. Treatment with recombinant mouse osteoactivin increased the amounts of collagen type I, MMP-3, and MMP-9 in mouse NIH-3T3 fibroblasts. The upregulated expression of these fibroblast marker proteins was significantly inhibited by heparin, but not by an integrin inhibitor, indicating that a heparin-binding motif in the extracellular domain might be an active site of osteoactivin. In osteoactivin-transgenic mice, denervation further enhanced expression of MMP-3 and MMP-9 in fibroblasts infiltrated into gastrocnemius muscle, compared with wild-type mice. Our present results suggest that osteoactivin might function as an activator for fibroblasts infiltrated into denervated skeletal muscles and play an important role in regulating degeneration/regeneration of extracellular matrix. sciatic neurectomy; Gpnmb family; C2C12 cells; NIH-3T3 cells; osteoactivin-transgenic mice DENERVATION (sciatic neurectomy) causes numerous changes in contractile, electrical, metabolic, and molecular properties of the muscle fiber membrane and sarcoplasm in hindlimb skeletal muscles (6, 10). Previous studies (21,22,32) have shown evidence that denervation alters interstitial spaces between muscle fibers: mononucleated cells are infiltrated into interstitial spaces of muscle fibers, and fibrosis occasionally occurs in the muscle. These findings suggest that the interaction between muscle fiber membrane and infiltrated cells might play an important role in degeneration or regeneration of denervated skeletal muscle. However, information on the interaction between the muscle fiber membrane and infiltrated cells is very little.To address this issue, we previously examined the expression of ϳ26,000 genes in rat gastrocnemius muscle atrophied by denervation or spaceflight using an Affymetrix DNA microarray...
Minimally invasive percutaneous endoscopic discectomy (PED) with a transforaminal approach under local anesthesia was started in the late 20th century. As the procedure requires a skin incision of only 8 mm, it is the least invasive disc surgery procedure at present, and owing to advances in instruments and optics, the use of this technique has gradually spread. In Japan, Dr. Dezawa from Teikyo University Mizonokuchi Hospital introduced this technique in 2003. Thanks to his efforts, the number of surgeons who can perform PED has increased, although the number of active PED surgeons is still only around 20. The first author (K.S.) started PED in 2010. In this review article, we explain the state-of-the-art PED transforaminal technique for minimally invasive disc surgery and present three successful cases.
History of elbow pain, pitcher position, catcher position, and longer training hours per week were associated with both types of pain. History of shoulder pain was associated with shoulder pain but not elbow pain. Age was associated with elbow pain but not shoulder pain.
In animal models, several ubiquitin ligases play an important role in skeletal muscle atrophy caused by unloading. In this study we examined protein ubiquitination and ubiquitin ligase gene expression in quadriceps femoris muscle from healthy volunteers after 20-day bedrest to clarify ubiquitin-dependent proteolysis in human muscles after unloading. During bedrest, thickness and cross-sectional area of the quadriceps femoris muscle decreased significantly by 4.6% and 3.7%, respectively. Ubiquitinated proteins accumulated in these atrophied human muscles. A real-time reverse transcription-polymerase chain reaction system showed that bedrest significantly upregulated expression of two ubiquitin ligase genes, Cbl-b and atrogin-1. We also performed DNA microarray analysis to examine comprehensive gene expression in the atrophied muscle. Bedrest mainly suppressed the expression of muscle genes associated with control of gene expression in skeletal muscle. Our results suggest that, in humans, Cbl-b- or atrogin-1-mediated ubiquitination plays an important role in unloading-induced muscle atrophy, and that unloading stress may preferentially inhibit transcriptional responses in skeletal muscle.
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