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Prepublished online as a Blood First Edition Paper on September 25, 2003; DOI 10.1182/blood-2003-05-1450. This Article Full Text (PDF) All Versions of this Article: 2003-05-1450v1 103/3/934    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 Kanters, E. Articles by de Winther, M. P J Search for Related Content PubMed PubMed Citation Articles by Kanters, E. Articles by de Winther, M. P J Related Collections Related Article in Blood Online Social Bookmarking                   What's this? Submitted May 8, 2003 Accepted September 16, 2003 Hematopoietic NF-B1 deficiency results in smaller atherosclerotic lesions with a more inflammatory phenotype Edwin Kanters, Marion J J Gijbels, Ingeborg van der Made, Monique N Vergouwe, Peter Heeringa, Georg Kraal, Marten H Hofker, and Menno P J de Winther* Department of Molecular Cell Biology and Immunology, VU Medical Center, Amsterdam, The Netherlands Department of Molecular Genetics, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands Department of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands Department of Immunology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands * Corresponding author; email: dewinther{at}gen.unimaas.nl. Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden macrophages in the vessel wall. One of the major transcription factors in inflammation is NF-B and we have studied its role in the development of atherosclerosis. Bone marrow from mice targeted in the NF-B1 gene encoding for the p50 subunit was used to reconstitute irradiated LDLR-/- mice as a model for atherosclerosis. After high fat feeding, mice deficient for NF-B1 developed 41% less atherosclerosis compared to control as judged by the size of the lesions. Furthermore, in the absence of NF-B1 the lesions were characterized by an inflammatory phenotype, contained increased numbers of small cells and were almost devoid of normal foam cells. In vitro studies using bone marrow derived macrophages showed that macrophages lacking p50 have a prolonged production of TNF in response to LPS, while other cytokines were also affected. Interestingly, uptake of oxidized LDL was greatly reduced in activated p50 deficient macrophages, probably due to a reduction in expression of scavenger receptor class A. The effects on atherosclerosis may be the result of changes in both cytokine production and uptake of modified lipoproteins, making p50 a pivotal regulator of atherogenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: NF-B activation in atherosclerosis: a friend or a foe? Ziad Mallat and Alain Tedgui Blood 2004 103: 754-755. [Full Text] [PDF] This article has been cited by other articles: Y. Etzion, A. Hackett, B. M. Proctor, J. Ren, B. Nolan, T. Ellenberger, and A. J. Muslin An Unbiased Chemical Biology Screen Identifies Agents That Modulate Uptake of Oxidized LDL by Macrophages Circ. Res., July 17, 2009; 105(2): 148 - 157. [Abstract] [Full Text] [PDF] S. X. L. Liu, R. Tian, H. Baskind, W. Hsueh, and I. G. 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