A comparative study of myostatin, follistatin and decorin expression in muscle of different origin

Abstract

Muscle regeneration supports muscle function in aging, and plays a role in the functional impairment caused by progressive neuromuscular diseases. Major substances controlling this process are growth factors and the extracellular matrix (ECM). Thus, follistatin is known to antagonize the function of several members of the TGF-β family of secreted signaling factors, including myostatin-the most powerful inhibitor of muscle growth characterized to date. Decorin-a small leucine-rich proteoglycan-traps myostatin and modulates its activity towards myogenic cells in the ECM. In addition, there are few reports concerning the regenerative muscle process of masseter muscles, which are of branchial arch origin, in mdx mice. Thus, in order to clarify the muscle regenerative process of masseter muscle, gene and protein expression of myostatin, follistatin and decorin were examined using the tibialis anterior (TA)muscle as a positive control. In both muscles, a gradual increase in mRNA myostatin, follistatin and decorin expression was detected, with the increase being greater in TA muscle than in masseter muscle. At 2 weeks, both muscles exhibited normal skeletal muscle cells. At 3 weeks, masseter muscle demonstrated scant areas of necrosis, whereas large necrotic zones were seen in TA muscle. At 4 weeks, the formation of necrotic tissue and presence of follistatin protein was observed clearly in masseter muscle. This result indicates that follistatin production is stimulated in the presence of necrosis. Interestingly, both muscles showed the same process of muscular formation, but with different time frames, which could be related to muscle origin.

Barx2 and Pax7 Have Antagonistic Functions in Regulation of Wnt Signaling and Satellite Cell Differentiation

“…For example, Dlk1, which is both a Wnt target gene and a Notch ligand, controls postnatal muscle growth and its ablation in the myogenic lineage results in postnatal growth retardation, reduced body and muscle weight, and impaired regeneration ; a phenotype that resembles that of Barx2 null mice. Fst is another Wnt target critical for muscle growth and regeneration . Notch3, which was elevated in Barx2−/− myoblasts, is suggested to be an inhibitor of satellite cell proliferation and self‐renewal via inhibition of Notch1 .…”

Influence of recombinant duck follistatin protein on embryonic muscle development and gene expressions

“…The results in this study showed that expression of MSTN was inhibited, which was similar with the results of in vivo study, supporting FST still worked on myoblasts. DCN, a out‐cellular ligand of TGFβpathway, also a competitor of FST (Hiroki et al., ), and its expression didn't show obvious changes. Expression of ACVR1 and ACVR2 in duck's myoblasts did not change when treated with FST suggesting it cannot regulate expression of ACVR1 and ACVR2.…”

Novel Therapies for the Management of Sports Injuries

“…They found that not only inhibition of MSTN, but also of activin (ACT) and proliferation of satellite cells are involved in follistatin-induced muscle hypertrophy [12]. Follistatin thus might offer a novel therapeutic strategy for muscular injuries and dystrophy by suppressing the progression of muscle degeneration and permitting skeletal muscle mass restoration [15]. However, before translating follistatin-based therapies from the bench to the bedside, clear mechanisms of how follistatin promotes muscle regeneration require extensive investigation.…”