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Myoblast Proliferation (myoblast + proliferation)
Selected AbstractsOestrogen receptor-alpha activation augments post-exercise myoblast proliferationACTA PHYSIOLOGICA, Issue 1 2010A. Thomas Abstract Aim:, Our laboratory has shown that oestrogen acts to augment myoblast (satellite cell) activation, proliferation and total number and that this may occur through an oestrogen receptor (OR)-mediated mechanism. The purpose of this study was to further investigate the mechanism of oestrogen influence on augmentation of post-exercise myoblast numbers through use of a specific OR-, agonist, propyl pyrazole triol (PPT). Methods:, Ovariectomized rats were used (n = 64) and separated into four groups: sham, oestrogen supplemented, agonist supplemented, and a combined oestrogen and agonist supplemented group. These groups were further subdivided into control (unexercised) and exercise groups. Surgical removal of white vastus and soleus muscles was performed 72 h post-exercise. Muscle samples were immunostained for the myoblast markers Pax7 and MyoD. Results:, A significant increase in total (Pax7-positive) and activated (MyoD-positive) myoblasts was found in all groups post-exercise. A further significant augmentation of total and activated myoblasts occurred in oestrogen supplemented, agonist supplemented and the combined oestrogen and agonist supplemented groups post-exercise in white vastus and soleus muscles relative to unsupplemented animals. Conclusion:, These results demonstrate that both oestrogen and the specific OR-, receptor agonist, PPT, can significantly and to similar degrees augment myoblast number and activation following exercise-induced muscle damage. This suggests that oestrogen acts through an OR-mediated mechanism to stimulate myoblast proliferation following exercise, with OR-, playing a primary role. [source] Dermatan sulfate exerts an enhanced growth factor response on skeletal muscle satellite cell proliferation and migrationJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2004Joan Villena Skeletal muscle regeneration is a complex process in which many agents are involved. When skeletal muscle suffers an injury, quiescent resident myoblasts called satellite cells are activated to proliferate, migrate, and finally differentiate. This whole process occurs in the presence of growth factors, the extracellular matrix (ECM), and infiltrating macrophages. We have shown previously that different proteoglycans, either present at the plasma membrane or the ECM, are involved in the differentiation process by regulating growth factor activity. In this article, we evaluated the role of glycosaminoglycans (GAGs) in myoblast proliferation and migration, using C2C12, a satellite cell-derived cell line. A synergic stimulatory effect on myoblast proliferation was observed with hepatocyte growth factor (HGF) and fibroblast growth factor type 2 (FGF-2), which was dependent on cell sulfation. The GAG dermatan sulfate (DS) enhanced HGF/FGF-2-dependent proliferation at 1,10 ng/ml. However, decorin, a proteoglycan containing DS, was unable to reproduce this enhanced proliferative effect. On the other hand, HGF strongly increased myoblast migration. The HGF-dependent migratory process required the presence of sulfated proteoglycans/GAGs present on the myoblast surface, as inhibition of both cell sulfation, and heparitinase (Hase) and chondroitinase ABC (Chabc) treatment of myoblasts, resulted in a very strong inhibition of cell migration. Among the GAGs analyzed, DS most increased HGF-dependent myoblast migration. Taken together, these findings showed that DS is an enhancer of growth factor-dependent proliferation and migration, two critical processes involved in skeletal muscle formation. J. Cell. Physiol. 198: 169,178, 2004© 2003 Wiley-Liss, Inc. [source] NDRG2, a novel regulator of myoblast proliferation, is regulated by anabolic and catabolic factorsTHE JOURNAL OF PHYSIOLOGY, Issue 7 2009Victoria C. Foletta Skeletal muscle tissue undergoes adaptive changes in response to stress and the genes that control these processes are incompletely characterised. NDRG2 (N-myc downstream-regulated gene 2), a stress- and growth-related gene, was investigated in skeletal muscle growth and adaption. While NDRG2 expression levels were found to be up-regulated in both differentiated human and mouse myotubes compared with undifferentiated myoblasts, the suppression of NDRG2 in C2C12 myoblasts resulted in slowed myoblast proliferation. The increased expression levels of the cell cycle inhibitors, p21 Waf1/Cip1 and p27 Kip1, and of various muscle differentiation markers in NDRG2-deficient myoblasts indicate that a lack of NDRG2 promoted cell cycle exiting and the onset of myogenesis. Furthermore, the analysis of NDRG2 regulation in C2C12 myotubes treated with catabolic and anabolic agents and in skeletal muscle from human subjects following resistance exercise training revealed NDRG2 gene expression to be down-regulated during hypertrophic conditions, and conversely, up-regulated during muscle atrophy. Together, these data demonstrate that NDRG2 expression is highly responsive to different stress conditions in skeletal muscle and suggest that the level of NDRG2 expression may be critical to myoblast growth and differentiation. [source] Interaction between myostatin and extracellular matrix componentsANIMAL SCIENCE JOURNAL, Issue 1 2010Takayuki MIURA ABSTRACT Myostatin, a member of the TGF-, superfamily, is a negative regulator of skeletal muscle mass. We have recently demonstrated that decorin binds to myostatin in vitro, and that immobilized decorin within the collagen matrix prevents myostatin-mediated inhibition of myoblast proliferation. However, little is known about other ECM molecules that bind to myostatin and modulate its activity. Thus, in the present study, we investigated the interaction of several other ECM molecules with myostatin. We here show that fibromodulin, fibronectin and laminin bind to myostatin in the presence of Zn2+ with a dissociation constant (KD) of 10,10,10,8 mol/L. Fibromodulin shows the highest affinity for myostatin among them. These results suggest that these ECM molecules may modulate myostatin activity like decorin does. [source] Construction of Skeletal Myoblast-Based Polyurethane Scaffolds for Myocardial RepairARTIFICIAL ORGANS, Issue 6 2007Matthias Siepe Abstract:, Intramyocardial transplantation of skeletal myoblasts augments postinfarction cardiac function. However, poor survival of injected cells limits this therapy. It is hypothesized that implantation of myoblast-based scaffolds would result in greater cell survival. Rat skeletal myoblasts were seeded on highly porous polyurethane (PU) scaffolds (7.5 × 7.5 × 2.0 mm). The effect of several scaffold pretreatments, initial cell densities, and culture periods was tested by DNA-based cell count and viability assessment. Seeded PU scaffolds were implanted on infarcted hearts and immunohistology was performed 4 weeks later. Precoating with laminin allowed the most favorable cell attachment. An initial inoculation with 5 × 106 cells followed by a 15-day culture period resulted in optimal myoblast proliferation. Four weeks after their implantation in rats, numerous myoblasts were found throughout the seeded patches although no sign of differentiation could be observed. This myoblast seeding technique on PU allows transfer of a large number of living myoblasts to a damaged myocardium. [source] Effects of maternal hyperthermia on myogenesis-related factors in developing upper limb,BIRTH DEFECTS RESEARCH, Issue 3 2009Jin Lee Abstract BACKGROUND: Maternal hyperthermia is one causative factor in various congenital anomalies in experimental animals and humans. In the present study, we assessed the effects of high temperature on limb myogenesis in mice. METHODS: Pregnant mice, C57BL/6 strain, were exposed to hyperthermia (43°C, 5 minutes) on embryonic day (ED) 8. Fetuses on ED 11, 13, 15, and 17 and neonates on postnatal day (PD) 1 were collected. To characterize the effects of hyperthermia on myogenesis-related factors Pax3, MyoD, myogenin, and myosin heavy chain (MyHC) during skeletal muscle development, we performed RT-PCR, western blotting, immunohistochemistry, and transmission electron microscopy. RESULTS: Pax3 gene expression was still detected on ED 13 in hyperthermia-exposed fetuses. The expression of MyoD protein was down-regulated in fetuses exposed to hyperthermia. In contrast, myogenin and MyHC protein expression were up-regulated on PD 1 and ED 17, respectively, in the group exposed to hyperthermia. Immunohistochemical analysis confirmed the findings from western blot analysis. Compared with control neonates, a TEM study revealed immature muscle fibers in PD 1 hyperthermia neonates. Thus, our studies showed that maternal hyperthermia induced delayed expression of Pax3 and inhibited expression of MyoD proteins, which are known to play important roles in migration of myogenic progenitor cells, and in myoblast proliferation. In addition, maternal hyperthermia also delayed the expression of myogenin protein for the formation of myotubes, and MyHC protein, which is one of the final muscle differentiation factors. CONCLUSION: Our data suggest that maternal hyperthermia delays limb myogenesis in part by disregulating the expression of key myogenesis-related factors. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. [source] | ||||||||||