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Inhibition of myogenesis enables adipogenic trans-differentiation in the C2C12 myogenic cell line

K Yeow1, B Phillips, C Dani

  • 1CNRS UMR 6548, Laboratory of Cellular and Molecular Physiology, University of Nice-Sophia Antipolis, Nice, France.

FEBS Letters
|October 10, 2001
PubMed

Insights

Inhibiting myogenesis in C2C12 cells with dominant negative MKK3 promotes adipocyte trans-differentiation. This process, enhanced by rosiglitazone and PPAR-gamma, is dependent on phosphoinositide-3 kinase signaling.

Area of Science:

  • Cell biology
  • Molecular biology
  • Biochemistry

Background:

  • C2C12 cells are a standard model for myogenesis research.
  • Understanding cell fate plasticity is crucial for regenerative medicine.

Purpose of the Study:

  • To investigate if inhibiting myogenesis facilitates C2C12 cell trans-differentiation into adipocytes.
  • To elucidate the molecular mechanisms involved in this trans-differentiation process.

Main Methods:

  • C2C12 cells were engineered to express dominant-negative MKK3 (DN MKK3).
  • Cells were treated with rosiglitazone and the PI3 kinase inhibitor LY294002.
  • Adipocyte formation was assessed through standard assays.

Main Results:

  • Expression of DN MKK3 enabled C2C12 cells to undergo adipocytic trans-differentiation in response to rosiglitazone.
  • Rosiglitazone's effect was potentiated by peroxisome proliferator-activated receptor-gamma (PPAR-gamma).
  • The PI3 kinase pathway was essential for this trans-differentiation, as shown by inhibition with LY294002.

Conclusions:

  • Preventing myogenesis via DN MKK3 expression promotes adipocytic trans-differentiation in C2C12 cells.
  • The process involves the activation of PPAR-gamma and is dependent on PI3 kinase signaling.

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