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Arch Physiol Biochem. 2017 Oct;123(4):249-253. doi: 10.1080/13813455.2017.1309052. Epub 2017 Apr 3.

Reduced expression of adipose triglyceride lipase decreases arachidonic acid release and prostacyclin secretion in human aortic endothelial cells.

Author information

1
a Institute of Molecular Biology and Biochemistry , Center of Molecular Medicine , Graz , Austria.
2
b Institute of Biomedical Science , University of Applied Sciences , Graz , Austria.
3
c Center for Medical Research, Core Facility Mass Spectrometry , Medical University Graz , Graz , Austria.

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.

KEYWORDS:

Arachidonic acid; adipose triglyceride lipase; eicosanoids; phospholipase

PMID:
28368219
PMCID:
PMC5942144
DOI:
10.1080/13813455.2017.1309052
[Indexed for MEDLINE]
Free PMC Article

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