Myoblasts differentiation

Duan, D., Z. Yan, Y. Yue, W. Ding, and J. F. Engelhardt. 2001. Enhancement of muscle gene delivery with pseudotyped adeno-associated virus type 5 correlates with myoblast differentiation. J Virol 75(16) 7662—71. 

A.C. Rapraeger, A. Krufka, and B.B. Olwin, Requirement of heparan sulfate for bFGF-mediated fibroblast growth and myoblast differentiation, Science 252, 1705-1708 (1991). 

Schmidt, C., Steiner, T., and Froesch, E. R., Preferential enhancement of myoblast differentiation by insulin-like growth foctors (IGF I and IGF II) in primary cultures of chicken embryonic cells. FEBS Lett. 161, 117-121 (1983). 

Immunostaining studies of cells isolated from the contracting areas within the EBs confirmed the presence of cardiac-specific proteins (MHC, sarcomeric a-actinin, des-min, cTnf, ANP). These studies also demonstrated the presence of early-cardiac morphology with a typical early-striated staining pattern. The cells, however, did not exhibit immunoreactivify with anti-nebuhn monoclonal antibodies (mAbs), a specific skeletal muscle sarcomeric protein shown to be expressed early in skeletal myoblast differentiation. 

Goodman, S., Deutzmann, R. and Nurcombe, V. (1989) Lo-comotory competence and laminin-specific cell surface binding sites are lost during myoblast differentiation. Development 106 795-802. 

The most striking physiological effect of GH is the stimulation of the longitudinal growth of bones. GH also increases bone mineral density after longitudinal growth ceases and epiphyses have closed. GH stimulates myoblast differentiation (in experimental animals), increases muscle mass (in human subjects with GH deficiency), increases glomerular filtration rate, and stimulates preadipocyte differentiation into adipocytes. 

Jost,J. P., Oakeley, E. J., Zhu, B., Benjamin, D., Thiry, S., Siegmann, M., andjost, Y. C. (2001). 5-Methylcytosine DNA glycosylase participates in the genome-wide loss of DNA methylation occurring during mouse myoblast differentiation. Nucleic Adds Res. 29, 4452-4461. 

In summary, these results demonstrate the involvement of NEU2 in the complex series of events leading to myoblast differentiation, although more information is needed in order to define the exact role played by this enzyme. For example, one important and open question is the identification of the possible subslrate(s) and product(s) of NEU2 in myofibers. 

S. Marchesini, Overexpression of cytosolic sialidase Neu2 induces myoblast differentiation in C2C12 cells, FEBS Lett, 547 (2003) 183-188. 

A. Fanzani, F. Colombo, R. Giuliani, A. Preti, and S. Marchesini, Insulin-like growth factor 1 signaling regulates cytosolic sialidase Neu2 expression during myoblast differentiation and hypertrophy, FEBS J., 273 (2006) 3709-3721. 

I. Jun, S. Jeong, and H. Shin, The stimulation of myoblast differentiation by electrically conductive sub-micron fibers. Biomaterials, 30, 2038-2047 (2009). 

Fig. 6a,b. ADPRT inhibitors block chick myoblast differentiation but not proliferation, a 3-amino-benzamide 3-aminobenzoate 3-methoxybenzamide 3-methoxybenzoate O nicotinamide, b 8 xM 3-aminobenzamide 10 mM 3-aminobenzamide 20 mM 3-aminobenzamide 5 mM 3-methoxybenzamide 18 mM 3-methoxybenzamide no inhibitor... 

Fig. 7a-d. Reversible inhibition of chick myoblast differentiation by ADPRT inhibitors and by nicotinamide deprivation. Reversible inhibition by 8 mAf 3-aminobenzamide (a,b), and by depletion of NAD levels (c,d)- a and c show myoblast cell fusion b and d show creatine phosphokinase activity. Control continuous presence of 8 mM 3-aminobenzamide the medium containing inhibitor was removed and replaced with medium from parallel control cultures of the same age at 44 h (O) or at 54 h ( ). In c and d myoblasts were cultured in nicotinamide-free medium. "No nicotinamide 1 mAf nicotinamide added at 0 h O l mAf nicotinamide added at 32-34 h of culture 1 mAf nicotinamide added at 52 h of culture... 

Devlin R, Emergson CP (1979) Coordinate accumulation of contractile protein mRNAs during myoblast differentiation. Dev Biol 69 202-216... 

It may be asked whether the changes in the pattern of poly(ADP-ribose) modified proteins are specific for myoblast differentiation. To answer this question we tested a myoblast clone that had lost its capacity to fuse. This clone (Nf-1) was isolated from the E63 myoblast cell line [1 ]. Cultures of Nf-1 were maintained for 8 days and were analyzed for poly(ADP-ribose) modified proteins. Figure 3 shows that the pattern of modified proteins isolated from the nonfusing variant is similar to that of prefusion E63 myoblasts (5 days). The 116 kD modified protein is present in both cultures, whereas the changes in poly(ADP-ribose) acceptor(s) accompanying differentiation are not observed. We have recently observed that the 116 kD modified protein is also formed if differentiation of E63 myoblasts is inhibited by DMSO or UV light. 

We propose that conditions altering the availability of NAD may be signaled to chromatin by the intermediacy of poly(ADP-ribose) (Fig. 2). The question is whether this signal operates imder physiological conditions. Some reports have provided direct evidence that NAD- depletion forced upon cells by incubation in nicotinamide-free medium, arrests poly(ADP-ribose) synthesis (5) and drastically alters chromatin functions (5-7). For example, DNA repair in response to a chemical carcinogen was arrested under these conditions, but could be reestablished with nicotinamide, which restored normal intracellular NAD- and poly(ADP-ribose) levels (5). Similarly, myoblast differentiation was reversibly inhibited either by nicotinamide starvation or by selective inhibition of poly(ADP-ribose) polymerase (7). These results illustrate that nutritional manipulation of... 

Cell proliferation and differentiation Electric conductivity was introduced by electrospinning carbon nanotubes with polyurethane. Myotube formation and myoblast differentiation were significantly increased with electrical stimulation apphed on the scaffolds. Sirivisoot et al. Composition... 

Fulco M, Cen Y, Zhao P, Hoffman EP, McBumey MW, Sauve AA, Sartorelli V (2008) Glucose restriction inhibits skeletal myoblast differentiation by activating SIRTl through AMPK-mediated regulation of Nampt. Dev Cell 14 661-673... 

Nandan, D., Clarke, E. P., Ball, E. H., and Sanwall, B. D., 1990, Ethyl-3,4-dihydroxybenzoate inhibits myoblast differentiation Evidence for an essential role of collagen, J. Cell Biol 110 1673-1679. 

Cells contain less hexosamine and sialic acid during myoblast differentiation, but D-glucose and D-galaetose accumulate the increase in these hexoses reflects the presence of components containing D-glucosyl-D-galactosylhydroxylysine on the cell surface as the myoblast reaches confluency. ... 

Buckingham, M. E., Caput, D., Cohen, A., Whalen, R. G., and Gros, F., 1974, The synthesis and stability of cytoplasmic messenger RNA during myoblast differentiation in culture, Proc. Natl. Acad. Sci. USA 71 1466. 

Levy-mishali, M., et al., 2009. Effect of scaffold stiffness on myoblast differentiation. Tissue Engineering. Part A 15 (4), 23-27. 

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