Selective modulation of microglial signal transduction by PACAP

Neuroreport. 2004 Jun 28;15(9):1469-74. doi: 10.1097/01.wnr.0000130541.29635.6f.

Abstract

We have investigated the possible effect of pituitary adenylate cyclase-activating polypeptide (PACAP) on signal transduction pathways associated with inflammatory activation of BV-2 mouse microglia cells. Pretreatment of the cells with PACAP resulted in a significant decrease in LPS- or IFNgamma-induced NO production as well as iNOS and IL-1beta mRNA levels. The inhibitory effect of PACAP appeared to be mediated through an increase in intracellular cAMP. PACAP inhibition of LPS-induced NO production was accompanied by inhibition of p38 MAPK activation, but not ERK, JNK, or NF-kappaB. IFNgamma-induced STAT-1 activation or IRF-1 induction was not significantly influenced by PACAP. Therefore, PACAP appears to suppress inflammatory activation of BV-2 microglia via specific inhibition of LPS-induced p38 MAPK pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Transformed
  • Lipopolysaccharides / pharmacology
  • Mice
  • Microglia / cytology
  • Microglia / drug effects*
  • Microglia / physiology*
  • Mitogen-Activated Protein Kinases / metabolism
  • Neuropeptides / pharmacology*
  • Neuroprotective Agents / pharmacology*
  • Nitric Oxide / metabolism
  • Pituitary Adenylate Cyclase-Activating Polypeptide
  • Signal Transduction / drug effects*
  • Signal Transduction / immunology
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Adcyap1 protein, mouse
  • Lipopolysaccharides
  • Neuropeptides
  • Neuroprotective Agents
  • Pituitary Adenylate Cyclase-Activating Polypeptide
  • Nitric Oxide
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases