RT info:eu-repo/semantics/article
T1 Neutral lipids are not a source of arachidonic acid for lipid mediator signaling in human foamy monocytes
A1 Guijas, Carlos
A1 Bermúdez Arias, Miguel Ángel
A1 Meana, Clara
A1 Astudillo del Valle, Alma María
A1 Pereira, Laura
A1 Fernández Caballero, Lidia
A1 Balboa García, María Ángeles
A1 Balsinde Rodríguez, Jesús
K1 Arachidonic acid
K1 Ácido araquidónico
K1 Mass spectrometry
K1 Espectrometría de masas
AB 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.
PB MDPI
SN 0214-4842
YR 2019
FD 2019
LK https://uvadoc.uva.es/handle/10324/55759
UL https://uvadoc.uva.es/handle/10324/55759
LA eng
NO Cells 2019, vol. 8, n. 8, 941
NO Producción Científica
DS UVaDOC
RD 24-nov-2024