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

Monika Riederer; Margarete Lechleitner; Harald Köfeler; Saša Frank

doi:10.1080/13813455.2017.1309052

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

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

Authors

Monika Riederer^{1

2}, Margarete Lechleitner¹, Harald Köfeler³, Saša Frank¹

Affiliations

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.

MeSH terms

Aorta / cytology
Aorta / metabolism*
Arachidonic Acid / metabolism*
Cells, Cultured
Endothelium, Vascular / cytology
Endothelium, Vascular / metabolism*
Epoprostenol / metabolism*
Humans
Lipase / antagonists & inhibitors
Lipase / genetics
Lipase / metabolism*
RNA, Small Interfering / genetics

Substances

RNA, Small Interfering
Arachidonic Acid
Epoprostenol
Lipase
PNPLA2 protein, human

Grants and funding

This work was supported by the Austrian Science Fund (FWF; grant P19473-B05 to S.F.) and the Frank Lanyar Foundation of the Medical University Graz, Austria (http://www.medunigraz.at/franz-lanyar-stiftung/) (grant 369 to S.F.). The funding sources had no involvement in study design; collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication.