TNF-alpha modulates cytokine and cytokine receptors in C2C12 myotubes

Cancer Lett. 2002 Jan 25;175(2):181-5. doi: 10.1016/s0304-3835(01)00717-0.

Abstract

Incubation of C2C12 differentiated myotubes in the presence of 1000 units/ml (100 ng/ml) of recombinant murine tumor necrosis factor-alpha (TNF-alpha) for up 6 h caused an important increase in mRNA content of the cytokine (10-fold at 6 h). The levels of expression of the two cytokine receptors were not changed by the cytokine at short-time intervals, but 48 h of treatment resulted in a decreased expression of TNFR1 (33%). Interestingly, the presence of the cytokine resulted in significant increases in mRNA content for the catabolic pro-inflammatory cytokines IL-6 (17-fold) and IFN-gamma (8-fold). Similarly, TNF-alpha also caused a moderate increased expression of different anti-inflammatory cytokines such as IL-9 (104%), IL-10 (24%) and IL-15 (47%). The results suggest that other cytokines may be involved in mediating TNF-alpha action in skeletal muscle and that anti-inflammatory cytokines may be released as a counter-regulatory mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD / drug effects
  • Antigens, CD / genetics*
  • Cell Line
  • Cytokines / drug effects
  • Cytokines / metabolism*
  • Gene Expression Regulation / drug effects*
  • Kinetics
  • Mice
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / metabolism*
  • Receptors, Cytokine / drug effects
  • Receptors, Cytokine / metabolism*
  • Receptors, Tumor Necrosis Factor / drug effects
  • Receptors, Tumor Necrosis Factor / genetics*
  • Receptors, Tumor Necrosis Factor, Type I
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Antigens, CD
  • Cytokines
  • Receptors, Cytokine
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Type I
  • Tumor Necrosis Factor-alpha