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

Journal article

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 p27(Kip1)), 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. Co...

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Authors: Sundlisaeter, E; Edelmann, R; Hol, J; Sponheim, J; Küchler, A

• Publication status: Published
• Journal: American journal of pathology
• Volume: 181
• Issue: 3
• Pages: 1099-1111
• Publication date: 2012-09-01
• DOI: 10.1016/j.ajpath.2012.06.003
• EISSN: 1525-2191
• ISSN: 0002-9440
• Language: English
• Keywords: Signal Transduction; Immunoglobulin J Recombination Signal Sequence-Binding Protein; Endothelial Cells; Neovascularization, Physiologic; Interleukins; Humans; Rats, Wistar; Receptor, Notch1; Wound Healing; Binding Sites; Genome, Human; Male; Animals; Female; Human Umbilical Vein Endothelial Cells; Protein Binding; Amyloid Precursor Protein Secretases; Rats; Cell Nucleus; Biological Markers; Down-Regulation; Genetic Loci; Dipeptides; Intercellular Signaling Peptides and Proteins; Calcium-Binding Proteins; Membrane Proteins