Expression of c‐jun/AP‐1 during myogenic differentiation in mouse C₂C₁₂ myoblasts

Abstract

Mitogen withdrawal triggers myogenic differentiation in skeletal myoblasts in culture. We have examined the expression of the proto‐oncogene c‐jun during this process in mouse C2C12 myoblasts. c‐jun belongs to a family of immediate early genes whose expression is activated in cultured cells in response to the addition of serum growth factors. Interestingly, expression of c‐jun was maintained in mouse C2C12 and rat L6 myoblasts undergoing myogenic differentiation under low‐serum conditions. Previously it has been reported that expression of c‐jun is downregulated during differentiation of C2 cells. However, our results using C2C12 cells, a subclone of the C2 line, show that c‐jun mRNA, protein and the activator‐protein 1 (AP‐1) DNA‐binding activity were easily detected in proliferating myoblasts and differentiated myotubes. Although overexpression of c‐jun has been shown to block myogenic differentiation in C2 cells, results presented here suggest that expression of c‐jun at physiological levels may not interfere with skeletal myogenesis.

Mechanisms to explain wasting of muscle and fat in cancer cachexia

“…In relation to AP-1 activation, TNF-a has been shown to increase c-jun expression in C2C12 cells [27]. Interestingly, overexpression of c-jun mimics the observed effect of TNF-a upon differentiation; indeed, it results in decreased myoblast differentiation [28]. Tumour mediators, proteolysis-inducing factor in particular, also seem to be able to increase NF-kB expression in cultured muscle cells, this possibly being linked with increased proteolysis [29].…”

Metabolic Oxidative Stress-induced HSP70 Gene Expression Is Mediated through SAPK Pathway

“…Following activation, JNK phosphorylates several transcription factors including activating transcription factor-2 (17), Elk-1 (18), Sap-1a (19), and c-Jun (20) which are involved in regulating numerous genes implicated in cell proliferation, transformation, differentiation, and DNA repair (21)(22)(23)(24). Recent studies also show that oxidative stress can activate HSF and increase HSP70 gene expression (25).…”

Involvement of histone H4 gene transcription factor 1 in downregulation of vimentin gene expression during skeletal muscle differentiation

“…It has been suggested that in muscle cells, AP1 and MyoD functionally antagonize each other through physical association between Jun and MyoD [12], so that upon muscle differentiation MyoD might block AP1‐dependent activation of the vimentin promoter. However, no decrease in c‐jun expression or AP1 binding activity was observed in C2C12 cells [13]. NF‐κB was reported to stimulate cell proliferation and to block muscle differentiation through activation of the cyclin D1 gene [14], suggesting that the positive effect of NF‐κB on the vimentin promoter may be counteracted during myogenesis.…”