English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/157795
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 | DATACITE
Exportar a otros formatos:


Foamy monocytes are enriched in cis-7-hexadecenoic fatty acid (16:1n-9), a possible biomarker for early detection of cardiovascular disease

AuthorsGuijas, Carlos ; Meana, Clara ; Astudillo, Alma M. ; Balboa, María A. ; Balsinde, Jesús
Issue Date2016
CitationCell Chemical Biology 23(6): 689-699 (2016)
AbstractHuman monocytes respond to arachidonic acid, a secretory product of endothelial cells, by activating the de novo pathway of fatty acid biosynthesis, resulting in the acquisition of a foamy phenotype due to accumulation of cytoplasmic lipid droplets. Recruitment of foamy monocytes to endothelium is a key step in the formation of atherosclerotic plaques. Here we describe that lipid droplets of foamy monocytes are enriched in a rather uncommon fatty acid, cis-7-hexadecenoic acid (16:1n-9), a positional isomer of palmitoleic acid. 16:1n-9 was found to possess an anti-inflammatory activity both in vitro and in vivo that is comparable with that of omega-3 fatty acids and clearly distinguishable from the effects of palmitoleic acid. Selective accumulation in neutral lipids of phagocytic cells of an uncommon fatty acid reveals an early phenotypic change that may provide a biomarker of proatherogenicity, and a potential target for intervention in the early stages of cardiovascular disease.
Publisher version (URL)https://doi.org/10.1016/j.chembiol.2016.04.012
Identifiersdoi: 10.1016/j.chembiol.2016.04.012
issn: 2451-9456
Appears in Collections:(IBGM) Artículos
Files in This Item:
File Description SizeFormat 
StimulatedOccurrence.pdf981,9 kBAdobe PDFThumbnail
Show full item record
Review this work

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