2026-07-21T14:57:27Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/96692024-09-27T09:05:33Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
González-Ramos, Silvia
author
Paz-García, Marta
author
Rius, Cristina
author
del Monte, Alberto
author
Rodriguez, Cristina
author
Fernández-García, Victoria
author
Andres, Vicente
author
Martinez-Gonzalez, Jose
author
Lasunción, Miguel A
author
Martín-Sanz, Paloma
author
Soehnlein, Oliver
author
Boscá, Lisardo
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Comunidad de Madrid (España)
funder
Deutsche Forschungsgemeinschaft (Alemania)
funder
Dutch Research Council (Holanda)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
2020-04-21T14:41:57Z
2020-04-21T14:41:57Z
2019-03
FASEB J. 2019; 33(3):3912-3921
10.1096/fj.201801231RR
1530-6860
0892-6638
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
30496704
http://hdl.handle.net/20.500.12105/9669
Atherosclerosis 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-κB 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.-González-Ramos, S., Paz-García, M., Rius, C., del Monte-Monge, A., Rodríguez, C., Fernández-García, V., Andrés, V., Martínez-González, J., Lasunción, M. A., Martín-Sanz, P., Soehnlein, O., Boscá, L. Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM-1.
eng
Cardiovascular disease
Innate immunity
Leukocyte
Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM-1
journal article
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EndothelialNOD1DirectsMyeloid_2019.pdf
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EndothelialNOD1DirectsMyeloid_2019.pdf.txt