Reduced expression of adipose triglyceride lipase decreases arachidonic acid release and prostacyclin secretion in human aortic endothelial cells
M Riederer, M Lechleitner, H Köfeler… - Archives of physiology …, 2017 - Taylor & Francis
M Riederer, M Lechleitner, H Köfeler, S Frank
Archives of physiology and biochemistry, 2017•Taylor & FrancisBackground: 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 …
(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 …
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 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.
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