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p38 mitogen-activated protein kinase activation is required for fibroblast growth factor-2-stimulated cell

P Maher1

  • 1Department of Cell Biology, Scripps Research Institute, La Jolla, California 92037, USA.

The Journal of Biological Chemistry
|June 11, 1999
PubMed

Insights

Basic fibroblast growth factor (FGF-2) triggers distinct cell responses via specific signaling pathways. FGF-2 activates extracellular signal-regulated kinases for differentiation and p38 mitogen-activated protein kinase for proliferation.

Area of Science:

  • Cell biology
  • Molecular signaling
  • Biochemistry

Background:

  • Basic fibroblast growth factor (FGF-2) influences diverse biological processes.
  • Distinct cell types exhibit varied responses to FGF-2, necessitating investigation into underlying mechanisms.

Purpose of the Study:

  • To elucidate the reasons behind differential cellular responses (differentiation vs. proliferation) to FGF-2.
  • To compare FGF receptor expression and downstream signaling pathways in distinct cell types.

Main Methods:

  • Comparative analysis of FGF receptor (FGFR) expression on PC12 cells (differentiation) and Swiss 3T3 fibroblasts (proliferation).
  • Examination of mitogen-activated protein kinase (MAPK) activation kinetics (ERK and p38) in response to FGF-2.
  • Utilizing specific MAPK inhibitors to assess their impact on FGF-2-induced differentiation and proliferation.

Main Results:

  • Both PC12 cells and Swiss 3T3 fibroblasts exclusively express FGFR1, indicating cell-specific FGFR1 signaling pathways.
  • FGF-2 activates extracellular signal-regulated kinases (ERK) similarly in both cell types; ERK inhibition blocks differentiation but not proliferation.
  • FGF-2 induces stronger, sustained p38 MAPK activation in fibroblasts compared to PC12 cells; p38 inhibition blocks proliferation but not differentiation.

Conclusions:

  • Cell type-specific signaling pathways downstream of FGFR1 mediate distinct cellular responses to FGF-2.
  • ERK activation is crucial for FGF-2-induced differentiation, while p38 MAPK activation is essential for FGF-2-mediated proliferation.

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