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Related Experiment Videos

TRAF2 expression in differentiated muscle

T K MacLachlan1, A Giordano

  • 1Department of Pathology, Sbarro Institute for Cancer Research and Molecular Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.

Journal of Cellular Biochemistry
|November 25, 1998
PubMed
Summary

Tumor necrosis factor receptor-associated factor 2 (TRAF2) protein is crucial for skeletal muscle integrity. TRAF2 stockpiling in differentiated muscle cells enhances anti-apoptotic responses, explaining muscle loss in TRAF2-deficient mice.

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Area of Science:

  • Muscle biology
  • Cellular signaling
  • Immunology

Background:

  • Tumor necrosis factor receptor-associated factor 2 (TRAF2) deficiency in mice leads to reduced skeletal muscle mass.
  • This muscle deficit is hypothesized to result from elevated circulating tumor necrosis factor (TNF).
  • TRAF2 plays a known role in TNF signaling pathways.

Purpose of the Study:

  • To investigate the role and expression of TRAF2 during skeletal muscle differentiation.
  • To elucidate the functional significance of TRAF2 in mature muscle cells.
  • To understand the molecular basis for muscle integrity defects in TRAF2 knockout models.

Main Methods:

  • Analysis of TRAF2 protein levels in developing mouse skeletal muscle.
  • In vitro differentiation of mouse myoblasts to myotubes.

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  • Assessment of basal and TNF-induced NF-kappaB activity in myoblasts and myotubes.

    • Main Results:

    • TRAF2 protein is highly expressed in terminally differentiated skeletal muscle.
    • TRAF2 protein levels significantly increase during in vitro myoblast differentiation.
    • TNF-induced NF-kappaB activity is markedly enhanced in myotubes compared to myoblasts due to TRAF2 accumulation.
    • NF-kappaB activity in myotubes suggests a potent, TRAF2-dependent anti-apoptotic mechanism.

    Conclusions:

    • TRAF2 protein is upregulated and functionally important in differentiated skeletal muscle.
    • Accumulation of TRAF2 in myotubes enhances TNF-induced NF-kappaB signaling, providing an anti-apoptotic effect.
    • These findings provide a molecular explanation for the skeletal muscle defects observed in traf2 knockout mice.