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Tumor necrosis factor-alpha gene transfer induces cachexia and inhibits muscle regeneration

Dario Coletti1, Viviana Moresi, Sergio Adamo

  • 1Brookdale Department of Molecular, Cell and Developmental Biology, Mount Sinai Medical School, New York, New York 10029, USA.

Genesis (New York, N.Y. : 2000)
|September 15, 2005
PubMed

Insights

Scientists created a new method to study muscle wasting using gene transfer of tumor necrosis factor-alpha (TNFalpha). This model effectively induces muscle atrophy and inhibits muscle regeneration in mice.

Area of Science:

  • Biomedical Research
  • Molecular Biology
  • Physiology

Background:

  • Chronic diseases elevate inflammatory cytokines, causing severe muscle wasting.
  • Existing in vivo cytokine models are limited for studying muscle wasting in new mouse mutants.

Purpose of the Study:

  • To develop a novel and simple in vivo model for inducing adult mouse skeletal muscle wasting.
  • To investigate the effects of murine tumor necrosis factor-alpha (mTNFalpha) on muscle atrophy and regeneration.

Main Methods:

  • Direct gene transfer of an expression vector encoding secreted murine tumor necrosis factor-alpha (mTNFalpha) into adult mice.
  • Monitoring body weight loss, Atrogin1 upregulation, and muscle atrophy.
  • Assessing the impact of mTNFalpha gene transfer on muscle regeneration following injury.

Main Results:

  • Gene transfer successfully induced elevated circulating mTNFalpha levels.
  • Induced significant body weight loss, Atrogin1 upregulation, and muscle atrophy, even in distant muscles.
  • Demonstrated significant inhibition of muscle regeneration after injury.

Conclusions:

  • TNFalpha is a potent inducer of cachexia (muscle wasting).
  • TNFalpha significantly inhibits myogenesis (muscle formation) in vivo.
  • The developed gene transfer model is effective for studying muscle wasting and TNFalpha's role.

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