Activation of p38 mitogen-activated protein kinase and activator protein-1 during the promotion of neurite extension of PC-12 cells by 15-deoxy-delta12,14-prostaglandin J2

Mol Pharmacol. 2003 Mar;63(3):607-16. doi: 10.1124/mol.63.3.607.

Abstract

15-Deoxy-Delta(12,14)-prostaglandin J(2) (15-deoxy-PGJ(2)), a naturally occurring ligand, activates the peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Activation of PPAR-gamma has been found to induce cell differentiation in such cells as adipose cells and macrophages. Herein, we investigated whether 15-deoxy-PGJ(2) has neuronal cell differentiation and possible underlying molecular mechanisms. Dopaminergic differentiating PC-12 cells treated with 15-deoxy-PGJ(2) (0.2 to 1.6 microM) alone showed measurable neurite extension and expression of neurofilament, a marker of cell differentiation. However, a much greater extent of neurite extension and expression of neurofilament was observed in the presence of NGF (50 ng/ml). In parallel with its increasing effect on the neurite extension and expression of neurofilament, 15-deoxy-PGJ(2) enhanced NGF-induced p38 MAP kinase expression and its phosphorylation in addition to the activation of transcription factor AP-1 in a dose-dependent manner. Moreover, pretreatment of 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(pyridyl)1H-imidazole (SB203580), a specific inhibitor of p38 MAP kinase, inhibited the promoting effect of 15-deoxy-PGJ(2) (0.8 microM) on NGF-induced neurite extension. This inhibition correlated well with the ability of SB203580 to inhibit the enhancing effect of 15-deoxy-PGJ(2) on the expression of p38 MAP kinase and activation of AP-1. The promoting ability of 15-deoxy-PGJ(2) did not occur through PPAR-gamma because synthetic PPAR-gamma agonist and antagonist did not change the neurite-promoting effect of 15-deoxy-PGJ(2). In addition, contrast to other cells (embryonic midbrain and neuroblastoma SK-N-MC cells), PPAR-gamma was not expressed in PC-12 cells. Other structure-related prostaglandins (PGD(2) and PGE(2)) acting via a cell surface G-protein-coupled receptor (GPCR) did not increase basal or NGF-induced neurite extension. Moreover, GPCR (PGE(2) and PGD(2) receptors) antagonists did not alter the promoting effect of 15-deoxy-PGJ(2) on neurite extension and activation of p38 MAP kinase, suggesting that the promoting effect of 15-deoxy-PGJ(2) may not be mediated by GPCR either. These data demonstrate that activation of p38 MAP kinase in conjunction with AP-1 signal pathway may be important in the promoting activity of 15-deoxy-PGJ(2) on the differentiation of PC-12 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Enzyme Activation
  • Imidazoles / pharmacology
  • Immunologic Factors / pharmacology*
  • Mitogen-Activated Protein Kinases / metabolism*
  • Nerve Growth Factors / physiology
  • Neurites / drug effects*
  • Neurites / metabolism
  • Neurofilament Proteins / biosynthesis
  • Neuropeptides / metabolism
  • PC12 Cells
  • Prostaglandin D2 / analogs & derivatives
  • Prostaglandin D2 / pharmacology*
  • Pyridines / pharmacology
  • Rats
  • Receptors, Cytoplasmic and Nuclear / biosynthesis
  • Signal Transduction / drug effects
  • Transcription Factor AP-1 / metabolism*
  • Transcription Factors / biosynthesis
  • p38 Mitogen-Activated Protein Kinases

Substances

  • 15-deoxy-delta(12,14)-prostaglandin J2
  • Anti-Inflammatory Agents, Non-Steroidal
  • Imidazoles
  • Immunologic Factors
  • Nerve Growth Factors
  • Neurofilament Proteins
  • Neuropeptides
  • Pyridines
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factor AP-1
  • Transcription Factors
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • SB 203580
  • Prostaglandin D2