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Public Library of Science, PLoS ONE, 7(6), p. e22327, 2011

DOI: 10.1371/journal.pone.0022327

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Myeloid IκBα Deficiency Promotes Atherogenesis by Enhancing Leukocyte Recruitment to the Plaques

Journal article published in 2011 by Pieter Goossens ORCID, P. Goossens (Pieter), Monique N. Vergouwe, Y. Vergouwe (Yvonne), Marion J. J. Gijbels, M. Gijbels (Marion), Danielle M. J. Curfs, Johannes H. G. van Woezik, D. M. J. Curfs (Danielle M.), J. H. G. van Woezik (Johannes H.), Marten A. Hoeksema ORCID, M. A. Hoeksema (Marten), Sofia Xanthoulea, S. Xanthoulea (Sofia), Pieter J. M. Leenen and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

abstractActivation of the transcription factor NF-κB appears to be involved in different stages of atherogenesis. In this paper we investigate the role of NF-κB inhibitor IκBα in atherosclerosis. Myeloid-specific deletion of IκBα 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 IκBα-deleted macrophages display enhanced adhesion to an in vitro endothelial cell layer, coinciding with an increased expression of the chemokine CCL5. Also, in vivo we found that IκBα del mice had more leukocytes adhering to the luminal side of the endothelial cell layers that cover the atherosclerotic plaques. Moreover, we introduce ER-MP58 in this paper as a new immunohistochemical tool for quantifying newly recruited myeloid cells in the atherosclerotic lesion. This staining confirms that in IκBα del mice more leukocytes are attracted to the plaques. In conclusion, we show that IκBα deletion in myeloid cells promotes atherogenesis, probably through an induced leukocyte recruitment to plaques.text