Neutral Lipids Are Not a Source of Arachidonic Acid for Lipid Mediator Signaling in Human Foamy Monocytes

Autor: Miguel A. Bermúdez, Alma M. Astudillo, Laura Pereira, Clara Meana, María A. Balboa, Carlos Guijas, Lidia Fernández-Caballero, Jesús Balsinde
Přispěvatelé: Ministerio de Economía y Competitividad (España), Universidad de Valladolid, Instituto de Salud Carlos III, Junta de Castilla y León
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Zdroj: Cells, Vol 8, Iss 8, p 941 (2019)
Cells
Volume 8
Issue 8
Digital.CSIC. Repositorio Institucional del CSIC
instname
UVaDOC. Repositorio Documental de la Universidad de Valladolid
ISSN: 2073-4409
Popis: Human monocytes exposed to free arachidonic acid (AA), a secretory product of endothelial cells, acquire a foamy phenotype which is due to the accumulation of cytoplasmic lipid droplets with high AA content. Recruitment of foamy monocytes to the inflamed endothelium contributes to the development of atherosclerotic lesions. In this work, we investigated the potential role of AA stored in the neutral lipids of foamy monocytes to be cleaved by lipases and contribute to lipid mediator signaling. To this end, we used mass spectrometry-based lipidomic approaches combined with strategies to generate monocytes with different concentrations of AA. Results from our experiments indicate that the phospholipid AA pool in monocytes is stable and does not change upon exposure of the cells to the external AA. On the contrary, the AA pool in triacylglycerol is expandable and can accommodate relatively large amounts of fatty acid. Stimulation of the cells with opsonized zymosan results in the expected decreases of cellular AA. Under all conditions examined, all of the AA decreases observed in stimulated cells were accounted for by decreases in the phospholipid pool; we failed to detect any contribution of the triacylglycerol pool to the response. Experiments utilizing selective inhibitors of phospholipid or triacylglyerol hydrolysis confirmed that the phospholipid pool is the sole contributor of the AA liberated by stimulated cells. Thus, the AA in the triacylglycerol is not a source of free AA for the lipid mediator signaling during stimulation of human foamy monocytes and may be used for other cellular functions.
This research was funded by the Spanish Ministry of Economy, Industry and Competitiveness, grant number SAF2016-80883-R. C.G., M.A.B. (Miguel A. Bermúdez), and L.P. were supported by predoctoral fellowships from the University of Valladolid, the Spanish Ministry of Science and Innovation, and the Regional Government of Castile and Leon, respectively. CIBERDEM is an initiative of Instituto de Salud Carlos III.
Databáze: OpenAIRE
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