TY - DATA T1 - Reduced expression of adipose triglyceride lipase decreases arachidonic acid release and prostacyclin secretion in human aortic endothelial cells PY - 2017/04/03 AU - Monika Riederer AU - Margarete Lechleitner AU - Harald Köfeler AU - Saša Frank UR - 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 DO - 10.6084/m9.figshare.4811080.v1 L4 - https://ndownloader.figshare.com/files/7959955 KW - Arachidonic acid KW - adipose triglyceride lipase KW - phospholipase KW - eicosanoids N2 - Background: 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. Objective: To examine the impact of ATGL on AA-release from cellular phospholipids (PL) and on prostacyclin secretion in human aortic endothelial cells (HAEC). Methods and results: 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 14C-AA from (14C-AA-labeled) HAEC. In A23187-stimulated ATGL silenced cells, this was accompanied by a decreased content of 14C-AA in cellular PL and a decreased secretion of prostacyclin (determined by 6-keto PGF1α EIA). Conclusions: In vascular endothelial cells, the efficiency of stimulus-induced AA release and prostacyclin secretion is dependent on ATGL. ER -