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G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle

Wright, Craig R., Brown, Erin L., Della-Gatta, Paul A., Ward, Alister C., Lynch, Gordon S. and Russell, Aaron P. 2014, G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle, Frontiers in physiology, vol. 5, Article number : 170, pp. 1-13, doi: 10.3389/fphys.2014.00170.

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Title G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle
Author(s) Wright, Craig R.ORCID iD for Wright, Craig R. orcid.org/0000-0001-7903-3144
Brown, Erin L.
Della-Gatta, Paul A.ORCID iD for Della-Gatta, Paul A. orcid.org/0000-0003-2231-8370
Ward, Alister C.ORCID iD for Ward, Alister C. orcid.org/0000-0001-7945-7975
Lynch, Gordon S.
Russell, Aaron P.ORCID iD for Russell, Aaron P. orcid.org/0000-0002-7323-9501
Journal name Frontiers in physiology
Volume number 5
Season Article number : 170
Start page 1
End page 13
Total pages 13
Publisher Frontiers Research Foundation
Place of publication Lausanne, Switzerland
Publication date 2014-05
ISSN 1664-042X
Keyword(s) C2C12
G-CSF
cytokine receptor
differentiation
duchenne muscular dystrophy
mdx
proliferation
skeletal muscle
Summary Granulocyte-colony stimulating factor (G-CSF) increases recovery of rodent skeletal muscles after injury, and increases muscle function in rodent models of neuromuscular disease. However, the mechanisms by which G-CSF mediates these effects are poorly understood. G-CSF acts by binding to the membrane spanning G-CSFR and activating multiple intracellular signaling pathways. Expression of the G-CSFR within the haematopoietic system is well known, but more recently it has been demonstrated to be expressed in other tissues. However, comprehensive characterization of G-CSFR expression in healthy and diseased skeletal muscle, imperative before implementing G-CSF as a therapeutic agent for skeletal muscle conditions, has been lacking. Here we show that the G-CSFR is expressed in proliferating C2C12 myoblasts, differentiated C2C12 myotubes, human primary skeletal muscle cell cultures and in mouse and human skeletal muscle. In mdx mice, a model of human Duchenne muscular dystrophy (DMD), G-CSF mRNA and protein was down-regulated in limb and diaphragm muscle, but circulating G-CSF ligand levels were elevated. G-CSFR mRNA in the muscles of mdx mice was up-regulated however steady-state levels of the protein were down-regulated. We show that G-CSF does not influence C2C12 myoblast proliferation, differentiation or phosphorylation of Akt, STAT3, and Erk1/2. Media change alone was sufficient to elicit increases in Akt, STAT3, and Erk1/2 phosphorylation in C2C12 muscle cells and suggest previous observations showing a G-CSF increase in phosphoprotein signaling be viewed with caution. These results suggest that the actions of G-CSF may require the interaction with other cytokines and growth factors in vivo, however these data provides preliminary evidence supporting the investigation of G-CSF for the management of muscular dystrophy.
Language eng
DOI 10.3389/fphys.2014.00170
Field of Research 110699 Human Movement and Sports Science not elsewhere classified
Socio Economic Objective 920116 Skeletal System and Disorders (incl. Arthritis)
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2014, Frontiers Research Foundation
Free to Read? Yes
Use Rights Creative Commons Attribution licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30067266

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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.