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c-Fos as a Regulator of Degranulation and Cytokine Production in FcRI-Activated Mast Cells¹

Yu-Nee Lee^*, Jan Tuckerman^,, Hovav Nechushtan, Gunter Schutz, Ehud Razin^2,* and Peter Angel

^* Department of Biochemistry, Hebrew University, Hadassah Medical School, and Oncology Department, Hadassah Hebrew University Medical Center, Jerusalem, Israel; and Division of Molecular Biology of the Cell I, and Division of Signal Transduction and Growth Control, Deutsches Krebsforschungszentrum, Heidelberg, Germany

The AP-1 complex is composed of c-Jun and c-Fos and is a key component in the regulation of proinflammatory genes. Mast cells play a significant role in the initiation of many inflammatory responses, such as allergy and allergy-associated diseases. In the present work, we characterized the role of c-Fos in mast cell function by investigating IL-3-dependent cell proliferation, degranulation capability, and cytokine expression in c-Fos-deficient mice. In c-Fos-deficient mast cells, we found that FcRI-mediated degranulation was significantly inhibited, which correlates with the reduced expression of SWAP-70, VAMP-7, and Synaptotagmin I genes, which are involved directly in the degranulation process. These findings show that c-Fos plays an important role in FcRI-mediated regulation of mast cell function.

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