10.6084/m9.figshare.4811080.v1 Monika Riederer Monika Riederer Margarete Lechleitner Margarete Lechleitner Harald Köfeler Harald Köfeler Saša Frank Saša Frank Reduced expression of adipose triglyceride lipase decreases arachidonic acid release and prostacyclin secretion in human aortic endothelial cells Taylor & Francis Group 2017 Arachidonic acid adipose triglyceride lipase phospholipase eicosanoids 2017-04-03 12:42:24 Figure https://tandf.figshare.com/articles/figure/Reduced_expression_of_adipose_triglyceride_lipase_decreases_arachidonic_acid_release_and_prostacyclin_secretion_in_human_aortic_endothelial_cells/4811080 <p><b>Background:</b> Vascular endothelial cells represent an important source of arachidonic acid (AA)-derived mediators involved in the generation of anti- or proatherogenic environments. Evidence emerged (in mast cells), that in addition to phospholipases, neutral lipid hydrolases as adipose triglyceride lipase (ATGL) also participate in this process.</p> <p><b>Objective:</b> To examine the impact of ATGL on AA-release from cellular phospholipids (PL) and on prostacyclin secretion in human aortic endothelial cells (HAEC).</p> <p><b>Methods and results:</b> siRNA-mediated silencing of ATGL promoted lipid droplet formation and TG accumulation in HAEC (nile red stain). ATGL knockdown decreased the basal and A23187 (calcium ionophore)-induced release of <sup>14</sup>C-AA from (<sup>14</sup>C-AA-labeled) HAEC. In A23187-stimulated ATGL silenced cells, this was accompanied by a decreased content of <sup>14</sup>C-AA in cellular PL and a decreased secretion of prostacyclin (determined by 6-keto PGF1α EIA).</p> <p><b>Conclusions:</b> In vascular endothelial cells, the efficiency of stimulus-induced AA release and prostacyclin secretion is dependent on ATGL.</p>