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FGF-2 blocks TGF-beta1-mediated suppression of Bcl-2 in normal melanocytes

Maria von Willebrand1, Klaus Köhler, Tuomo Alanko

  • 1Department of Dermatology, Helsinki University Central Hospital, University of Helsinki, PB160, 00029 HUS, Finland. marie.vonwillebrand@helsinki.fi

Experimental Dermatology
|March 3, 2005
PubMed

Insights

Fibroblast growth factor-2 (FGF-2) prevents transforming growth factor-beta1 (TGF-beta1)-induced apoptosis in normal melanocytes by maintaining Bcl-2 levels. This mechanism is specific to normal melanocytes, not melanoma cells.

Area of Science:

  • Cell Biology
  • Dermatology
  • Molecular Biology

Background:

  • Normal melanocytes rely on basement membrane support for survival.
  • Nevus and melanoma cells exhibit altered survival mechanisms, thriving in dermis or on collagen gels.
  • Transforming growth factor-beta1 (TGF-beta1) induces apoptosis in normal melanocytes on collagen gels, an effect counteracted by fibroblast growth factor-2 (FGF-2).

Purpose of the Study:

  • To elucidate the mechanisms by which FGF-2 counteracts TGF-beta1-induced apoptosis in melanocytes cultured on collagen gel.

Main Methods:

  • Investigated signal transduction pathways from TGF-beta1 receptors to SMAD2/3 proteins.
  • Assessed the impact of TGF-beta1 and FGF-2 on Bcl-2 protein levels in normal melanocytes, nevus cells, and melanoma cells cultured on collagen gel.

Main Results:

  • FGF-2 did not affect TGF-beta1 signal transduction to SMAD2/3 proteins.
  • TGF-beta1 reduced Bcl-2 levels in normal melanocytes, while FGF-2 reversed this reduction.
  • TGF-beta1 did not decrease Bcl-2 levels in nevus or melanoma cells, and FGF-2 had no effect on Bcl-2 in these cells.

Conclusions:

  • Reduced Bcl-2 levels are implicated in TGF-beta1-induced apoptosis of normal melanocytes on collagen gels.
  • FGF-2 mitigates TGF-beta1-induced apoptosis by preventing the reduction of anti-apoptotic Bcl-2 protein.

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