Mitogen-activated protein kinase activation through Fc epsilon receptor I and stem cell factor receptor is differentially regulated by phosphatidylinositol 3-kinase and calcineurin in mouse bone marrow-derived mast cells

J Immunol. 1999 Feb 15;162(4):2087-94.

Abstract

Aggregation of high affinity FcR for IgE (Fc epsilon RI) on mast cells activates intracellular signal transduction pathways, including the activation of protein tyrosine kinases, phosphatidylinositol 3-kinase (PI3-kinase), and protein kinase C. Binding of stem cell factor (SCF) to its receptor (SCFR, c-Kit) on mast cells also induces increases in intrinsic tyrosine kinase activity and activation of PI3-kinase. Although ligation of both receptors induces Ras and Raf-1 activation, the downstream consequences of these early activation events are not well defined, except for the activation of extracellular signal-regulated kinases (ERK). Addition of Ag (OVA) to mouse bone marrow-derived mast cells (BMMC) sensitized with anti-OVA IgE triggers the activation of three members of the mitogen-activated protein (MAP) kinase family, c-Jun amino-terminal kinase (JNK), p38 MAP kinase (p38), and extracellular signal-regulated kinases. SCF similarly activates all three MAP kinases. Wortmannin, an inhibitor of PI3-kinase, inhibited both Fc epsilon RI- and SCFR-mediated JNK activation and partially inhibited Fc epsilon RI, but not SCFR-mediated p38 activation. Cyclosporin A inhibited Fc epsilon RI-mediated JNK and p38 activation, but did not affect the activation of these kinases when stimulated through the SCFR. Wortmannin and cyclosporin A inhibited Fc epsilon RI-mediated production of TNF-alpha and IL-4 in addition to serotonin release in BMMC. These results indicate that both PI3-kinase and calcineurin may contribute to the regulation of cytokine gene transcription and the degranulation response by modulating JNK activity in BMMC.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Androstadienes / pharmacology
  • Animals
  • Bone Marrow Cells / drug effects
  • Bone Marrow Cells / enzymology*
  • Bone Marrow Cells / metabolism
  • Calcineurin / physiology*
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
  • Cyclosporine / pharmacology
  • Enzyme Activation / drug effects
  • Female
  • Flavonoids / pharmacology
  • Interleukin-4 / antagonists & inhibitors
  • Interleukin-4 / biosynthesis
  • JNK Mitogen-Activated Protein Kinases
  • Mast Cells / drug effects
  • Mast Cells / enzymology*
  • Mast Cells / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinases*
  • Molecular Sequence Data
  • Phosphatidylinositol 3-Kinases / physiology*
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins c-kit / metabolism
  • Proto-Oncogene Proteins c-kit / physiology*
  • Proto-Oncogene Proteins*
  • Receptor Aggregation / drug effects
  • Receptors, IgE / metabolism
  • Receptors, IgE / physiology*
  • Serotonin / metabolism
  • Serotonin Antagonists / pharmacology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Wortmannin
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Androstadienes
  • Flavonoids
  • Proto-Oncogene Proteins
  • Receptors, IgE
  • Serotonin Antagonists
  • Tumor Necrosis Factor-alpha
  • Interleukin-4
  • Serotonin
  • Cyclosporine
  • Proto-Oncogene Proteins c-kit
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Calcium-Calmodulin-Dependent Protein Kinases
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • Calcineurin
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one
  • Wortmannin