L6E9 Myoblasts Are Deficient of Myostatin and Additional TGF-β Members Are Candidates to Developmentally Control Their Fiber Formation

This work provides evidence that the robust myoblast differentiation observed in L6E9 cells is causally linked to deficiency of myostatin, which, conversely, has been found to be expressed in C2C12 cells. However, despite the absence of endogenous myostatin, L6E9 myoblasts expressed functional Activ...

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Bibliographic Details
Published in:Journal of biomedicine & biotechnology 2010-01, Vol.2010 (2010), p.1-9
Main Authors: Rossi, Stefania, Stoppani, Elena, Gobbo, Massimiliano, Caroli, Anna, Fanzani, Alessandro
Format: Article
Language:English
Subjects:
Activin Receptors, Type II - genetics
Activin Receptors, Type II - metabolism
Animals
Biological and medical sciences
Cell Line
Follistatin - genetics
Follistatin - metabolism
Gene Knockdown Techniques
Histocytochemistry
Humans
Medical sciences
Mice
Mice, Inbred C57BL
Muscle Fibers, Skeletal - cytology
Muscle Fibers, Skeletal - metabolism
Myoblasts - cytology
Myoblasts - metabolism
Myostatin - deficiency
Myostatin - genetics
Myostatin - metabolism
Pharmacology. Drug treatments
Rats
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Transforming Growth Factor beta - metabolism
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Summary:This work provides evidence that the robust myoblast differentiation observed in L6E9 cells is causally linked to deficiency of myostatin, which, conversely, has been found to be expressed in C2C12 cells. However, despite the absence of endogenous myostatin, L6E9 myoblasts expressed functional Activin receptors type II (ActRIIs) and follistatin as well as the highly related TGF-β members Activins and GDF11, suggesting that in this cell line the regulation of fiber size might be under the control of multiple regulators regardless of myostatin. In line with this hypothesis, delivery of a dominant-negative ActRIIb form or the increase of follistatin, as obtained via Trichostatin treatment or stable transfection of a short human follistatin form, enhanced the L6E9 cell differentiation and further increased the size of myotubes, suggesting that L6E9 myoblasts provide a spontaneous myostatin knock-out in vitro model to study TGF-β ligands involved in developmental regulation of fiber size.
ISSN:1110-7243
1110-7251
DOI:10.1155/2010/326909