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Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
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
Doi: 10.1080/13813455.2017.1309052
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- Führende Autor*innen der Med Uni Graz
- Frank Sasa
- Riederer Monika
- Co-Autor*innen der Med Uni Graz
- Köfeler Harald
- Lechleitner Margarete
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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 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). In vascular endothelial cells, the efficiency of stimulus-induced AA release and prostacyclin secretion is dependent on ATGL.
- Find related publications in this database (using NLM MeSH Indexing)
- 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
- Find related publications in this database (Keywords)
- Arachidonic acid
- adipose triglyceride lipase
- phospholipase
- eicosanoids