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The alarmin IL-33 is a notch target in quiescent endothelial cells.

Am J Pathol.. 2012-09;  181(3):1099-111
Sundlisaeter E, Edelmann RJ, Hol J, Sponheim J, KÜchler AM, Weiss M, Udalova IA, Midwood KS, Kasprzycka M, Haraldsen G. Laboratory for Immunohistochemistry and Immunopathology, Department of Pathology, Oslo University Hospital, and University of Oslo, Oslo, Norway‡ Norwegian Center for Stem Cell Research and Institute of Immunology, Oslo University Hospital, and University of Oslo, Norway† Department of Internal Medicine, Asker and Bærum Hospital, Vestre Viken Hospital Trust, Rud, Norway§ Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskele
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摘要

The molecular mechanisms that drive expression of the alarmin interleukin-33 (IL-33) in endothelial cells are unknown. Because nuclear IL-33 is a marker of endothelial cell quiescence (corroborated in this study by coexpression of cyclin-dependent kinase inhibitor p27Kip1), we hypothesized that Notch signaling might be involved in regulating IL-33 expression. Activation of Notch1 by immobilized Notch ligands was sufficient to induce nuclear IL-33 expression in cultured endothelial cells. Conversely, IL-33 expression was inhibited by the Γ-secretase inhibitor DAPT or by inhibiting the function of Dll4, Jagged1, Notch1, or the canonical Notch transcription factor RBP-JΚ. Insensitivity to cycloheximide... More

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