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SHR Neuro Krebs Kardio Lipid

Riederer, M; Lechleitner, M; Köfeler, H; Frank, S.
Reduced expression of adipose triglyceride lipase decreases arachidonic acid release and prostacyclin secretion in human aortic endothelial cells.
Arch Physiol Biochem. 2017; 123(4): 249-253. [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Autor/innen der Med Uni Graz:
Frank Saša
Köfeler Harald
Lechleitner Margarete
Riederer Monika
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Number of Figures: 3
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Abstract:
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. To examine the impact of ATGL on AA-release from cellular phospholipids (PL) and on prostacyclin secretion in human aortic endothelial cells (HAEC). 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). In vascular endothelial cells, the efficiency of stimulus-induced AA release and prostacyclin secretion is dependent on ATGL.

Find related publications in this database (Keywords)
Arachidonic acid
adipose triglyceride lipase
phospholipase
eicosanoids
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