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Nerve growth factor induces survival and differentiation through two distinct signaling cascades in PC12 cells

L J Klesse1, K A Meyers, C J Marshall

  • 1Center for Developmental Biology, University of Texas, Southwestern Medical Center, Dallas 75235-9133, USA.

Oncogene
|May 13, 1999
PubMed

Insights

Nerve growth factor (NGF) triggers PC12 cell differentiation via the ras/ERK pathway, but not survival. Phosphoinositide 3-kinase (PI3K) signaling is crucial for NGF-induced cell survival.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Neuroscience

Background:

  • Nerve growth factor (NGF) is known to induce differentiation and survival in rat PC12 pheochromocytoma cells.
  • The extracellular signal-regulated kinase (ERK) cascade is a key signaling pathway implicated in mediating NGF's effects.

Purpose of the Study:

  • To investigate the specific roles of the ras/ERK pathway in NGF-mediated PC12 cell differentiation, survival, and proliferation.
  • To elucidate the signaling mechanisms underlying NGF's functions in PC12 cells.

Main Methods:

  • Generation of recombinant adenoviruses to express wild-type, dominant-negative, and constitutively active forms of ras/ERK pathway intermediates.
  • Utilized PC12 cell cultures treated with NGF and manipulated signaling pathways.
  • Assessed cell differentiation, survival, and proliferation in response to genetic and chemical modulations.

Main Results:

  • PC12 cell differentiation induced by NGF requires the activity of the ras/ERK pathway.
  • Inhibition of the ras/ERK pathway did not affect PC12 cell survival or proliferation.
  • Phosphoinositide 3-kinase (PI3K) signaling, not ras/ERK, is essential for PC12 cell survival in serum-free conditions.
  • Constitutively active raf and MEK could promote survival, but only through PI3K activation.

Conclusions:

  • NGF utilizes distinct signaling pathways to mediate its diverse functions in PC12 cells.
  • The ras/ERK pathway is critical for NGF-induced differentiation, while PI3K signaling is necessary for survival.
  • Cross-talk between ERK and PI3K pathways may exist, particularly in promoting cell survival.

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