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

@article{Hoene2013Interleukin6PM,
  title={Interleukin-6 promotes myogenic differentiation of mouse skeletal muscle cells: role of the STAT3 pathway.},
  author={Miriam Hoene and Heike Runge and H. U. H{\"a}ring and Erwin D. Schleicher and Cora Weigert},
  journal={American journal of physiology. Cell physiology},
  year={2013},
  volume={304 2},
  pages={
          C128-36
        }
}
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… 
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36 References

JAK/STAT signaling and human in vitro myogenesis

Insight is provided into JAK/STAT signaling in human skeletal muscle development, and recent observations in rodents are confirmed.

JAK1–STAT1–STAT3, a key pathway promoting proliferation and preventing premature differentiation of myoblasts

It is demonstrated that Janus kinase 1 (JAK1) is required for myoblast proliferation and that it also functions as a checkpoint to prevent myoblasts from premature differentiation.

JAK2/STAT2/STAT3 Are Required for Myogenic Differentiation*

A novel role for the JAK2/STAT2/ STAT3 pathway in myogenic differentiation is revealed, suggesting that this pathway could also promote differentiation by regulating signaling molecules known to be involved inMyogenic differentiation.

SOCS-3 Induces Myoblast Differentiation*

Overexpression of SOCS-3 cDNA significantly increased transcriptional activation of the 2.0-kb skeletal α-actin promoter in differentiating C2C12 myoblasts, indicating that SOCs-3 can contribute to the myoblast differentiation process in the absence of IGF-I.

Reciprocal Inhibition between MyoD and STAT3 in the Regulation of Growth and Differentiation of Myoblasts*

The results suggest that the development of muscle cells is regulated by the coordination of cytokine signals and intrinsic transcription factors.

Inhibition of Myoblast Differentiation by Tumor Necrosis Factor α Is Mediated by c-Jun N-terminal Kinase 1 and Leukemia Inhibitory Factor*

Studies with cell lines expressing MyoD:ER chimera and lacking JNK1 or JNK2 genes indicate that JNK 1 activity mediates the effects of TNFα on myoblast proliferation and differentiation, and TNF α promotes myOBlast proliferation through J NK1 and prevents my oblast differentiation through JNK3-mediated secretion of LIF.

Leukemia inhibitory factor blocks early differentiation of skeletal muscle cells by activating ERK.

Interleukin-6 is an essential regulator of satellite cell-mediated skeletal muscle hypertrophy.

Cardiotrophin-1 Maintains the Undifferentiated State in Skeletal Myoblasts*

Exogenous systemic expression of CT-1 mediated by adenoviral vector delivery increased the number of myonuclei in normal post-natal mouse skeletal muscle and also delayed skeletal muscle regeneration induced by cardiotoxin injection.

p38 MAPK-induced nuclear factor-kappaB activity is required for skeletal muscle differentiation: role of interleukin-6.

This study provides the first evidence of a crosstalk between p38 MAPK and NF-kappaB signaling pathways during myogenesis, with IL-6 being one of the effectors of this promyogenic mechanism.