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Regulation of granulocyte colony-stimulating factor and its receptor in skeletal muscle is dependent upon the type of inflammatory stimulus

Wright, Craig Robert, Brown, Erin Louise, Della Gatta, Paul A., Fatouros, Ioannis G., Karagounis, Leonidas G., Terzis, Gerasimos, Mastorakos, Georgios, Michailidis, Yannis, Mandalidis, Dimitris, Spengos, Kontantinos, Chatzinikolaou, Athanasios, Methenitis, Spiros, Draganidis, Dimitrios, Jamurtas, Athanasios Z. and Russell, Aaron Paul 2015, Regulation of granulocyte colony-stimulating factor and its receptor in skeletal muscle is dependent upon the type of inflammatory stimulus, Journal of interferon and cytokine research, vol. 35, no. 9, pp. 710-719.

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Title Regulation of granulocyte colony-stimulating factor and its receptor in skeletal muscle is dependent upon the type of inflammatory stimulus
Author(s) Wright, Craig RobertORCID iD for Wright, Craig Robert orcid.org/0000-0001-7903-3144
Brown, Erin Louise
Della Gatta, Paul A.ORCID iD for Della Gatta, Paul A. orcid.org/0000-0003-2231-8370
Fatouros, Ioannis G.
Karagounis, Leonidas G.
Terzis, Gerasimos
Mastorakos, Georgios
Michailidis, Yannis
Mandalidis, Dimitris
Spengos, Kontantinos
Chatzinikolaou, Athanasios
Methenitis, Spiros
Draganidis, Dimitrios
Jamurtas, Athanasios Z.
Russell, Aaron PaulORCID iD for Russell, Aaron Paul orcid.org/0000-0002-7323-9501
Journal name Journal of interferon and cytokine research
Volume number 35
Issue number 9
Start page 710
End page 719
Total pages 10
Publisher Mary Ann Liebert
Place of publication Larchmont, N.Y.
Publication date 2015-09-01
ISSN 1557-7465
Summary The cytokine granulocyte colony-stimulating factor (G-CSF) binds to its receptor (G-CSFR) to stimulate hematopoietic stem cell mobilization, myelopoiesis, and the production and activation of neutrophils. In response to exercise-induced muscle damage, G-CSF is increased in circulation and G-CSFR has recently been identified in skeletal muscle cells. While G-CSF/G-CSFR activation mediates pro- and anti-inflammatory responses, our understanding of the role and regulation in the muscle is limited. The aim of this study was to investigate, in vitro and in vivo, the role and regulation of G-CSF and G-CSFR in skeletal muscle under conditions of muscle inflammation and damage. First, C2C12 myotubes were treated with lipopolysaccharide (LPS) with and without G-CSF to determine if G-CSF modulates the inflammatory response. Second, the regulation of G-CSF and its receptor was measured following eccentric exercise-induced muscle damage and the expression levels we investigated for redox sensitivity by administering the antioxidant N-acetylcysteine (NAC). LPS stimulation of C2C12 myotubes resulted in increases in G-CSF, interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNFα) messenger RNA (mRNA) and an increase in G-CSF, IL-6, and MCP-1 release from C2C12 myotubes. The addition of G-CSF following LPS stimulation of C2C12 myotubes increased IL-6 mRNA and cytokine release into the media, however it did not affect MCP-1 or TNFα. Following eccentric exercise-induced muscle damage in humans, G-CSF levels were either marginally increased in circulation or remain unaltered in skeletal muscle. Similarly, G-CSFR levels remained unchanged in response to damaging exercise and G-CSF/G-CSFR did not change in response to NAC. Collectively, these findings suggest that G-CSF may cooperate with IL-6 and potentially promote muscle regeneration in vitro, whereas in vivo aseptic inflammation induced by exercise did not change G-CSF and G-CSFR responses. These observations suggest that different models of inflammation produce a different G-CSF response.
Language eng
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 ©2015, Mary Ann Liebert
Persistent URL http://hdl.handle.net/10536/DRO/DU:30077711

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