| First Author | Goossens P | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 7 | Pages | e22327 |
| PubMed ID | 21814576 | Mgi Jnum | J:174920 |
| Mgi Id | MGI:5141523 | Doi | 10.1371/journal.pone.0022327 |
| Citation | Goossens P, et al. (2011) Myeloid IkappaBalpha deficiency promotes atherogenesis by enhancing leukocyte recruitment to the plaques. PLoS One 6(7):e22327 |
| abstractText | Activation of the transcription factor NF-kappaB appears to be involved in different stages of atherogenesis. In this paper we investigate the role of NF-kappaB inhibitor IkappaBalpha in atherosclerosis. Myeloid-specific deletion of IkappaBalpha 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 IkappaBalpha-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 IkappaBalpha(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 IkappaBalpha(del) mice more leukocytes are attracted to the plaques. In conclusion, we show that IkappaBalpha deletion in myeloid cells promotes atherogenesis, probably through an induced leukocyte recruitment to plaques. |
