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Blood, 1 February 2004, Vol. 103, No. 3, pp. 934-940. Prepublished online as a Blood First Edition Paper on September 25, 2003; DOI 10.1182/blood-2003-05-1450. This Article Full Text 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 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 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 Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Phagocytes Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Hematopoietic NF-B1 deficiency results in small atherosclerotic lesions with an 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 From the Department of Molecular Cell Biology and Immunology, VU Medical Center, Amsterdam; and the Departments of Molecular Genetics, Pathology, and Immunology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands. 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 nuclear factor B (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 feeding the mice a high-fat diet, those deficient in NF-B1 had a 41% lower rate of atherosclerosis than control mice, as judged by the sizes 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 (BM)-derived macrophages showed that macrophages lacking p50 had a prolonged production of tumor necrosis factor (TNF) in response to lipopolysaccharide (LPS), and other cytokines were also affected. Interestingly, the uptake of oxidized low-density lipoprotein (LDL) was greatly reduced in activated p50-deficient macrophages, probably because of a reduction in the expression of scavenger receptor class A. The effects on atherosclerosis might have resulted from the changes in cytokine production and the uptake of modified lipoproteins, making p50 a pivotal regulator of atherogenesis. (Blood. 2004;103:934-940) 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. 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