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The Journal of Immunology, 1999, 162: 2087-2094.
Copyright © 1999 by The American Association of Immunologists

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 Cells1

Tamotsu Ishizuka*,{dagger}, Kosuke Chayama*,{dagger}, Katsuyuki Takeda*,{dagger}, Eckard Hamelmann*,{dagger}, Naohiro Terada*,{dagger}, Gordon M. Keller{ddagger}, Gary L. Johnson*,{dagger} and Erwin W. Gelfand2,*,{dagger}

* Division of Basic Sciences, Department of Pediatrics, {dagger} Program in Molecular Signal Transduction, and {ddagger} Division of Immunology, Department of Medicine, National Jewish Medical and Research Center, Denver, CO 80206

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.




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