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>