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. Attached Files Name Description MIMEType Size Downloads wright-GCSFdoes-2014.pdf Published version application/pdf 3.77MB 100 Title G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle Author(s) Wright, Craig R. orcid.org/0000-0001-7903-3144 Brown, Erin L. Della-Gatta, Paul A. orcid.org/0000-0003-2231-8370 Ward, Alister C. orcid.org/0000-0001-7945-7975 Lynch, Gordon S. 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? 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