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Reduced expression of adipose triglyceride lipase decreases arachidonic acid release and prostacyclin secretion in human aortic endothelial cells.
Arch Physiol Biochem. 2017 Apr 03;:1-5
Authors: Riederer M, Lechleitner M, Köfeler H, Frank S
Abstract
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 (14)C-AA from ((14)C-AA-labeled) HAEC. In A23187-stimulated ATGL silenced cells, this was accompanied by a decreased content of (14)C-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.
PMID: 28368219 [PubMed - as supplied by publisher]
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