Calcium-dependent expression of TNF-alpha in neural cells is mediated by the calcineurin/NFAT pathway

Mol Cell Neurosci. 2006 Apr;31(4):692-701. doi: 10.1016/j.mcn.2005.12.008. Epub 2006 Feb 2.

Abstract

We report induction of TNF-alpha via the calcium/calcineurin/NFAT pathway in PC12 neural cells. In PC12, expression of TNF-alpha mRNA, protein and TNF-alpha gene promoter activity was induced by co-stimulation with phorbol ester and either calcium ionophore A23187 or the L-type Voltage Gated Calcium Channel agonist Bay K 8644. Pre-treatment with calcineurin inhibitors CsA or FK506 inhibited the dominant calcium-dependent component of this induction, limiting it to the level achieved with phorbol ester alone. Promoter activation by Bay was abolished by nifedipine, a specific inhibitor of L-type Voltage Gated Calcium Channels. Exogenous NFAT protein transactivated the TNF-alpha promoter, and the peptide VIVIT-a specific inhibitor of calcineurin/NFAT binding-blocked calcium-inducible transactivation of the TNF-alpha promoter. Given proposed functions of TNF-alpha in spatial learning, memory and the pathogenesis of neurodegenerative diseases, the data presented suggest an important role for calcineurin/NFAT signaling in these key neurological processes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / pharmacology
  • Animals
  • Calcimycin / pharmacology
  • Calcineurin / metabolism*
  • Calcium / metabolism*
  • Calcium Channel Agonists / pharmacology
  • Calcium Signaling / physiology
  • Cycloheximide / pharmacology
  • Cyclosporine / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation
  • Humans
  • Immunosuppressive Agents / pharmacology
  • Ionophores / pharmacology
  • NFATC Transcription Factors / metabolism*
  • Neurons* / drug effects
  • Neurons* / metabolism
  • Oligopeptides / metabolism
  • PC12 Cells
  • Protein Synthesis Inhibitors / pharmacology
  • Rats
  • Tacrolimus / pharmacology
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription, Genetic
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Calcium Channel Agonists
  • Enzyme Inhibitors
  • Immunosuppressive Agents
  • Ionophores
  • NFATC Transcription Factors
  • Oligopeptides
  • Protein Synthesis Inhibitors
  • Tumor Necrosis Factor-alpha
  • VIVIT peptide
  • Calcimycin
  • 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
  • Cyclosporine
  • Cycloheximide
  • Calcineurin
  • Tetradecanoylphorbol Acetate
  • Calcium
  • Tacrolimus