Roles of Rac and p38 kinase in the activation of cytosolic phospholipase A2 in response to PMA

Biochem J. 2005 Jun 1;388(Pt 2):527-35. doi: 10.1042/BJ20041614.

Abstract

The roles of Rac and p38 kinase in the activation of cPLA2 (cytosolic PLA2) in Rat-2 fibroblasts were investigated. In the present study, we found that PMA activates cPLA2 by a Rac-p38 kinase-dependent pathway. Consistent with this, Rac, if activated, was shown to stimulate cPLA2 in a p38 kinase-dependent manner. In another experiment to understand the signalling mechanism by which the Rac-p38 kinase cascade mediates cPLA2 activation in response to PMA, we observed that PMA-induced cPLA2 translocation to the perinuclear region is completely inhibited by the expression of Rac1N17 or treatment with SB203580 (inhibitor of p38 kinase), suggesting that Rac-p38 kinase cascade acts in this instance by mediating the translocation of cPLA2. The mediatory role of p38 kinase in cPLA2 activation was further demonstrated after a treatment with anisomycin, a very effective activator of p38 kinase. Consistent with the mediatory role of p38 kinase in stimulating cPLA2, anisomycin induced the translocation and activation of cPLA2 in a p38 kinase-dependent manner.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anisomycin / pharmacology
  • Cell Line
  • Cytosol / enzymology
  • Enzyme Activation
  • Fibroblasts / enzymology
  • Phospholipases A / metabolism*
  • Phospholipases A2
  • Protein Transport
  • Rats
  • Signal Transduction
  • Tetradecanoylphorbol Acetate / pharmacology*
  • p38 Mitogen-Activated Protein Kinases / metabolism*
  • rac GTP-Binding Proteins / metabolism*

Substances

  • Anisomycin
  • p38 Mitogen-Activated Protein Kinases
  • Phospholipases A
  • Phospholipases A2
  • rac GTP-Binding Proteins
  • Tetradecanoylphorbol Acetate