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Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM-1

AuthorsGonzález-Ramos, Silvia; Paz-García, Marta; Rius, Cristina; Monte-Monge, Alberto del; Rodríguez, Cristina ; Fernández-García, Victoria; Andrés, Vicente; Martínez-González, José; Lasunción, Miguel A.; Martín-Sanz, Paloma ; Soehnlein, Oliver; Boscá, Lisardo
KeywordsCardiovascular disease
Innate immunity
Issue DateMar-2019
PublisherFederation of American Societies for Experimental Biology
CitationFASEB Journal - Federation of American Societies for Experimental Biology 33(3): 3912 (2019)
AbstractAtherosclerosis is a chronic disease characterized by vascular lipid retention and inflammation, and pattern recognition receptors (PRRs) are important contributors in early stages of the disease. Given the implication of the intracellular PRR nucleotide-binding oligomerization domain 1 (NOD1) in cardiovascular diseases, we investigated its contribution to early atherosclerosis. We evidenced NOD1 induction in atherosclerotic human and mouse tissues, predominantly in vascular endothelial cells. Accordingly, NOD1 genetic inactivation in Apoe-/- mice reduced not only atherosclerosis burden, but also monocyte and neutrophil accumulation in atheromata. Of note, in the presence of either peptidoglycan or oxidized LDLs, endothelial NOD1 triggered VCAM-1 up-regulation through the RIP2-NF-¿B axis in an autocrine manner, enhancing firm adhesion of both sets of myeloid cells to the inflamed micro- and macrovasculature in vivo. Our data define a major proatherogenic role for endothelial NOD1 in early leukocyte recruitment to the athero-prone vasculature, thus introducing NOD1 as an innovative therapeutic target and potential prognostic molecule
Publisher version (URL)http://dx.doi.org/10.1096/fj.201801231RR
Identifiersdoi: 10.1096/fj.201801231RR
issn: 0892-6638
e-issn: 1530-6860
Appears in Collections:(IIBB) Artículos
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