Glucocorticoid inhibits growth factor-induced differentiation of hippocampal progenitor HiB5 cells

J Neurochem. 2001 Dec;79(5):1013-21. doi: 10.1046/j.1471-4159.2001.00634.x.

Abstract

In the present study, we investigated the effect of glucocorticoid on neuronal differentiation of hippocampal progenitor HiB5 cells. Dexamethasone (DEX), a synthetic glucocorticoid, inhibited platelet-derived growth factor (PDGF)-induced differentiation of HiB5 cells. The inhibitory effect of DEX was antagonized by RU486, a glucocorticoid receptor (GR) antagonist, indicating the GR-mediated processes. Nestin mRNA level was decreased and midsize neurofilament (NF-M) mRNA level was increased as a function of neuronal differentiation. DEX significantly blocked PDGF-induced down-regulation of nestin mRNA level, and up-regulation of NF-M mRNA level, which were similar to those of undifferentiated cells. DEX inhibited PDGF-induced activation of cyclic AMP-responsive element binding protein (CREB) and AP-1, suggesting that glucocorticoid interfered with signal transduction cascades linking the PDGF receptor and downstream transcription factors. Indeed, DEX reduced PDGF-induced phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2). Tyrosine phosphatase inhibitor reversed the effect of DEX on ERK1/2. In accordance with this finding, blockage of ERK1/2 signaling pathway with PD098059, a potent inhibitor for Ras/ERK pathway, mimicked the inhibitory effect of DEX on differentiation processes. Taken together, these results indicate that glucocorticoid inhibits PDGF-induced differentiation of hippocampal progenitor HiB5 cells by inhibiting the ERK1/2 signaling cascade via a tyrosine phosphatase-dependent mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Southern
  • Blotting, Western
  • Cell Differentiation / drug effects
  • Cell Line
  • Dexamethasone / pharmacology
  • Glucocorticoids / pharmacology*
  • Growth Substances / pharmacology*
  • Hippocampus / cytology*
  • Hippocampus / drug effects
  • Humans
  • Luciferases / metabolism
  • Neurites / drug effects
  • Phosphorylation
  • Platelet-Derived Growth Factor / metabolism
  • Protein Tyrosine Phosphatases / metabolism
  • Receptors, Glucocorticoid / biosynthesis
  • Receptors, Glucocorticoid / drug effects
  • Receptors, Mineralocorticoid / biosynthesis
  • Receptors, Mineralocorticoid / drug effects
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / drug effects
  • Stem Cells / drug effects*
  • Transfection

Substances

  • Glucocorticoids
  • Growth Substances
  • Platelet-Derived Growth Factor
  • Receptors, Glucocorticoid
  • Receptors, Mineralocorticoid
  • Dexamethasone
  • Luciferases
  • Protein Tyrosine Phosphatases