English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/123815
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:
Title

A major role for RCAN1 in atherosclerosis progression

AuthorsMéndez-Barbero, Nerea; Esteban, Vanesa; Alfranca, Arántzazu; Rodríguez, Cristina; Andrés, Vicente; Martínez-González, José; Redondo, Juan Miguel ; Campanero, Miguel R.
Issue Date2013
PublisherWiley-VCH
CitationEMBO Molecular Medicine 5(12): 1901-1917 (2013)
AbstractAtherosclerosis is a complex inflammatory disease involving extensive vascular vessel remodelling and migration of vascular cells. As RCAN1 is implicated in cell migration, we investigated its contribution to atherosclerosis. We show RCAN1 induction in atherosclerotic human and mouse tissues. Rcan1 was expressed in lesional macrophages, endothelial cells and vascular smooth muscle cells and was induced by treatment of these cells with oxidized LDLs (oxLDLs). Rcan1 regulates CD36 expression and its genetic inactivation reduced atherosclerosis extension and severity in Apoe-/- mice. This effect was mechanistically linked to diminished oxLDL uptake, resistance to oxLDL-mediated inhibition of macrophage migration and increased lesional IL-10 and mannose receptor expression. Moreover, Apoe-/-Rcan1-/- macrophages expressed higher-than-Apoe-/- levels of anti-inflammatory markers. We previously showed that Rcan1 mediates aneurysm development and that its expression is not required in haematopoietic cells for this process. However, transplantation of Apoe-/-Rcan1-/- bone-marrow (BM) cells into Apoe-/- recipients confers atherosclerosis resistance. Our data define a major role for haematopoietic Rcan1 in atherosclerosis and suggest that therapies aimed at inhibiting RCAN1 expression or function might significantly reduce atherosclerosis burden. © 2013 The Authors. Published by John Wiley and Sons, Ltd on behalf of EMBO.
DescriptionThis is an open access article under the terms of the Creative Commons Attribution License.-- et al.
Publisher version (URL)http://dx.doi.org/10.1002/emmm.201302842
URIhttp://hdl.handle.net/10261/123815
DOI10.1002/emmm.201302842
Identifiersdoi: 10.1002/emmm.201302842
e-issn: 1757-4684
issn: 1757-4676
Appears in Collections:(CIC) Artículos
(IIBM) Artículos
Files in This Item:
File Description SizeFormat 
RCAN1.pdf3,3 MBAdobe PDFThumbnail
View/Open
Show full item record
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.