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Cellular Plasmalogen Content Does Not Influence Arachidonic Acid Levels or Distribution in Macrophages: A Role for Cytosolic Phospholipase A2γ in Phospholipid Remodeling
Open AccessArticle

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

1
Instituto de Biología y Genética Molecular, Consejo Superior de Investigaciones Científicas (CSIC), Universidad de Valladolid, 47003 Valladolid, Spain
2
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work and share first authorship.
Cells 2019, 8(8), 941; https://doi.org/10.3390/cells8080941
Received: 4 August 2019 / Revised: 16 August 2019 / Accepted: 18 August 2019 / Published: 20 August 2019
(This article belongs to the Special Issue Phospholipids: Dynamic Lipid Signaling in Health and Diseases)
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. View Full-Text
Keywords: arachidonic acid; mass spectrometry; lipid signaling; inflammation; phospholipase A2; monocytes/macrophages arachidonic acid; mass spectrometry; lipid signaling; inflammation; phospholipase A2; monocytes/macrophages
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Guijas, C.; Bermúdez, M.A.; Meana, C.; Astudillo, A.M.; Pereira, L.; Fernández-Caballero, L.; Balboa, M.A.; Balsinde, J. Neutral Lipids Are Not a Source of Arachidonic Acid for Lipid Mediator Signaling in Human Foamy Monocytes. Cells 2019, 8, 941.

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