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Intracellular interaction of newly synthesized nerve growth factor and its receptors

Hiroshi Nomoto1, Hisako Notsu, Yuka Kato

  • 1Laboratory of Biochemistry, College of Pharmaceutical Sciences, Matsuyama University, Ehime 790-8578, Japan. hnomoto@cc.matsuyama-u.ac.jp

Biochemical and Biophysical Research Communications
|February 16, 2013
PubMed

Insights

Autocrine nerve growth factor (NGF) signaling may occur intracellularly. In PC84 cells, NGF receptors (TrkA, p75NTR) and signaling molecule MAP kinase were phosphorylated, suggesting internal ligand-receptor interaction.

Area of Science:

  • Cell biology
  • Neuroscience
  • Molecular signaling

Background:

  • Autocrine signaling involves ligand and receptor synthesis within the same cell.
  • Intracellular mechanisms of autocrine signaling, particularly for nerve growth factor (NGF), remain poorly understood.
  • Previous work showed intracellular precursor phosphorylation and MAP kinase activation in PC84 cells.

Purpose of the Study:

  • To investigate the intracellular interaction of NGF and its receptors (TrkA, p75NTR) in PC84 cells.
  • To explore the localization and form of NGF receptors within autocrine cells.
  • To determine if intracellular signaling occurs independently of extracellular NGF-receptor binding.

Main Methods:

  • Utilized PC84 cells, a mutant PC12 cell line engineered to express NGF.
  • Analyzed the localization and precursor status of TrkA and p75NTR receptors.
  • Assessed MAP kinase phosphorylation under conditions blocking extracellular NGF-receptor interaction using anti-NGF antibody.

Main Results:

  • NGF receptors TrkA and p75NTR were predominantly found as precursors within PC84 cells.
  • The majority of p75NTR localized intracellularly.
  • MAP kinase phosphorylation was observed even when extracellular NGF-TrkA/p75NTR interactions were blocked.

Conclusions:

  • Results suggest that NGF receptors exist mainly as precursors and are localized intracellularly.
  • Intracellular phosphorylation of MAP kinase indicates signaling activation.
  • These findings support the hypothesis of intracellular NGF-receptor interaction in autocrine signaling.

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