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Hoene, M. ; Runge, H.* ; Häring, H.-U. ; Schleicher, E.D. ; Weigert, C.

Interleukin-6 promotes myogenic differentiation of mouse skeletal muscle cells: Role of the STAT3 pathway.

Am. J. Physiol.-Cell Physiol. 304, 128-136 (2013)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Hoene M, Runge H, Haring HU, Schleicher ED, Weigert C. Interleukin-6 promotes myogenic differentiation of mouse skeletal muscle cells: role of the STAT3 pathway. Am J Physiol Cell Physiol 304: C128-C136, 2013. First published October 31, 2012; doi:10.1152/ajpcell.00025.2012.-Myogenic differentiation of skeletal muscle cells is characterized by a sequence of events that include activation of signal transducer and activator of transcription 3 (STAT3) and enhanced expression of its target gene Socs3. Autocrine effects of IL-6 may contribute to the activation of the STAT3-Socs3 cascade and thus to myogenic differentiation. The importance of IL-6 and STAT3 for the differentiation process was studied in C2C12 cells and in primary mouse wild-type and IL-6(-/-) skeletal muscle cells. In differentiating C2C12 myoblasts, the upregulation of IL-6 mRNA expression and protein secretion started after increased phosphorylation of STAT3 on tyrosine 705 and increased mRNA expression of Socs3 was observed. Knockdown of STAT3 and IL-6 mRNA in differentiating C2C12 myoblasts impaired the expression of the myogenic markers myogenin and MyHC IIb and subsequently myotube fusion. However, the knockdown of IL-6 did not prevent the induction of STAT3 tyrosine phosphorylation. The IL-6-independent activation of STAT3 was verified in differentiating primary IL-6(-/-) myoblasts. The phosphorylation of STAT3 and the expression levels of STAT3, Socs3, and myogenin during differentiation were comparable in the primary myoblasts independent of the genotype. However, IL-6(-/-) cells failed to induce MyHC IIb expression to the same level as in wild-type cells and showed reduced myotube formation. Supplementation of IL-6 could partially restore the fusion of IL-6(-/-) cells. These data demonstrate that IL-6 depletion during myogenic differentiation does not reduce the activation of the STAT3-Socs3 cascade, while IL-6 and STAT3 are both necessary to promote myotube fusion.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Socs3 ; Stat3 ; Differentiation ; Igf-i ; Il-6(-/-) Myoblasts; Leukemia Inhibitory Factor ; Messenger-rna Expression ; Necrosis-factor-alpha ; Myoblast Differentiation ; Protein-kinase ; I Receptor ; Exercise ; Metabolism ; Glucose ; Humans
ISSN (print) / ISBN 0363-6143
e-ISSN 1522-1563
Zeitschrift American Journal of Physiology - Cell Physiology
Quellenangaben Band: 304, Heft: 2, Seiten: 128-136 Artikelnummer: , Supplement: ,
Verlag American Physiological Society
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research and Metabolic Diseases (IDM)