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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 (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 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. Social Bookmarking                   What's this? Submitted September 25, 2003 Accepted November 25, 2003 Transcriptional profiling of IKK2/NF-B- and p38 MAP kinase-dependent gene expression in TNF--stimulated primary human endothelial cells Dorothee Viemann, Matthias Goebeler, Sybille Schmid, Kerstin Klimmek, Clemens Sorg, Stephan Ludwig, and Johannes Roth* Experimental Dermatology, University Hospital Muenster, Muenster, Germany; Pediatrics, University Hospital Muenster, Muenster, Germany Dermatology, University Hospital of Wuerzburg, Wuerzburg, Germany Integrated Functional Genomics, University of Muenster, Muenster, Germany Experimental Dermatology, University Hospital Muenster, Muenster, Germany Institute of Molecular Medicine, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany * Corresponding author; email: rothj{at}uni-muenster.de. Inflammatory stimulation of endothelial cells (EC) by tumor necrosis factor (TNF-) involves activation of NF-B and p38 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 > 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 IKK2/NF-B activation while a minor number was additionally modulated by p38. Furthermore, genes suppressed by IKK2/NF-B were newly identified. Real-time 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. M. Gillooly, M. A. Pattoli, T. L. Taylor, L. Chen, L. Cheng, K. R. Gregor, G. S. Whitney, V. Susulic, S. H. Watterson, J. Kempson, et al. 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