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Blood, 1 May 2004, Vol. 103, No. 9, pp. 3365-3373. Prepublished online as a Blood First Edition Paper on January 8, 2004; DOI 10.1182/blood-2003-09-3296. This Article Full Text Full Text (PDF) Supplemental Tables All Versions of this Article: 2003-09-3296v1 103/9/3365    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Viemann, D. Articles by Roth, J. Search for Related Content PubMed PubMed Citation Articles by Viemann, D. Articles by Roth, J. Related Collections Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Gene Expression Genomics Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Transcriptional profiling of IKK2/NF-B— and p38 MAP kinasedependent gene expression in TNF-—stimulated primary human endothelial cells Dorothee Viemann, Matthias Goebeler, Sybille Schmid, Kerstin Klimmek, Clemens Sorg, Stephan Ludwig, and Johannes Roth From the Departments of Experimental Dermatology and Pediatrics, University Hospital Münster, Münster, Germany; Department of Dermatology, University Hospital of Würzburg, Würzburg, Germany; Integrated Functional Genomics, University of Münster, Münster, Germany; Institute of Molecular Medicine, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Inflammatory stimulation of endothelial cells by tumor necrosis factor (TNF-) involves activation of nuclear factor B (NF-B) and p38 mitogen-activated protein (MAP) kinase signaling pathways. A reliable analysis of the gene expression program elicited by TNF- and its assignment to distinct signaling pathways is not available. A sophisticated analysis of oligonucleotide microarrays covering more than 13 000 genes allowed definition of the TNF--regulated endothelial gene expression profile and novel TNF--induced genes. Virtually all TNF--inducible genes were dependent on IB kinase 2 (IKK2)/NF-B activation, whereas a minor number was additionally modulated by p38. Furthermore, genes suppressed by IKK2/NF-B were newly identified. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry confirmed reliability of data. Thus, these results define a list of primary candidates for targeted modulation of endothelial functions during inflammation. 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