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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 κB (NF-κB), and we have studied its role in the development of atherosclerosis. Bone marrow from mice targeted in the NF-κB1 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-κB1 had a 41% lower rate of atherosclerosis than control mice, as judged by the sizes of the lesions. Furthermore, in the absence of NF-κB1, 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 …