有哪些信誉好的足球投注网站myeloid iκbα deficiency promotes atherogenesis by enhancing leukocyte recruitment to the plaques骨髓iκbα缺乏促进动脉粥样化形成提高白细胞招募斑块.pdfVIP
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myeloid iκbα deficiency promotes atherogenesis by enhancing leukocyte recruitment to the plaques骨髓iκbα缺乏促进动脉粥样化形成提高白细胞招募斑块
Myeloid IkBa Deficiency Promotes Atherogenesis by Enhancing Leukocyte Recruitment to the Plaques 1 1 1,2 1 Pieter Goossens , Monique N. Vergouwe , Marion J. J. Gijbels , Danielle M. J. Curfs , Johannes H. G. 1 1 1 3 4 van Woezik , Marten A. Hoeksema , Sofia Xanthoulea , Pieter J. M. Leenen , Rudolf A. Rupec , Marten H. 5 1 Hofker , Menno P. J. de Winther * 1 Department of Molecular Genetics, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands, 2 Department of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands, 3 Department of Immunology, Erasmus University Medical Center, Rotterdam, The Netherlands, 4 Department of Dermatology, Ludwig-Maximilian-University, Munich, Germany, 5 Department of Pathology and Medical Biology, Medical Biology Section, Molecular Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands Abstract Activation of the transcription factor NF-kB appears to be involved in different stages of atherogenesis. In this paper we investigate the role of NF-kB inhibitor IkBa in atherosclerosis. Myeloid-specific deletion of IkBa results in larger and more advanced lesions in LDL-R-deficient mice without affecting the compositional phenotype of the plaques or systemic inflammatory markers in the plasma. We show that IkBa-deleted macrophages display enhanced adhesion to an in vitro endothelial cell layer, coinciding with an increased expression of the chemokine CCL5. Also,
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