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 75 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? Yes Use Rights Persistent URL http://hdl.handle.net/10536/DRO/DU:30067266 Document type: Journal Article Collections: School of Exercise and Nutrition Sciences School of Medicine Centre for Physical Activity and Nutrition Research Open Access Collection Molecular and Medical Research Related Links Link Description Connect to Elements publication management system Go to link with your DU access privileges   Connect to published version Go to link with your DU access privileges   Author URL Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. 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. Versions Version Filter Type Thu, 06 Nov 2014, 12:37:18 EST Tue, 09 Dec 2014, 08:51:50 EST Tue, 09 Dec 2014, 13:21:23 EST Tue, 09 Dec 2014, 13:43:37 EST Thu, 18 Dec 2014, 10:27:01 EST Thu, 18 Dec 2014, 10:29:15 EST Thu, 18 Dec 2014, 14:25:20 EST Fri, 06 Feb 2015, 11:32:06 EST Wed, 14 Oct 2015, 13:55:23 EST Fri, 26 Aug 2016, 15:17:05 EST Mon, 05 Sep 2016, 16:04:42 EST Wed, 07 Sep 2016, 07:55:15 EST Filtered Full Citation counts:   Cited 2 times in TR Web of Science Cited 4 times in Scopus Search Google Scholar Access Statistics: 182 Abstract Views, 76 File Downloads  -  Detailed Statistics Created: Tue, 09 Dec 2014, 08:51:50 EST

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.