脂肪甘油三酯脂肪酶表达降低会减少人主动脉内皮细胞中花生四烯酸的释放和前列环素的分泌。
Reduced expression of adipose triglyceride lipase decreases arachidonic acid release and prostacyclin secretion in human aortic endothelial cells.
作者信息
Riederer Monika, Lechleitner Margarete, Köfeler Harald, Frank Saša
机构信息
a Institute of Molecular Biology and Biochemistry , Center of Molecular Medicine , Graz , Austria.
b Institute of Biomedical Science , University of Applied Sciences , Graz , Austria.
出版信息
Arch Physiol Biochem. 2017 Oct;123(4):249-253. doi: 10.1080/13813455.2017.1309052. Epub 2017 Apr 3.
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 C-AA from (C-AA-labeled) HAEC. In A23187-stimulated ATGL silenced cells, this was accompanied by a decreased content of C-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.
背景
血管内皮细胞是花生四烯酸（AA）衍生介质的重要来源，这些介质参与抗动脉粥样硬化或促动脉粥样硬化环境的形成。有证据表明（在肥大细胞中），除了磷脂酶外，中性脂质水解酶如脂肪甘油三酯脂肪酶（ATGL）也参与了这一过程。
目的
研究ATGL对人主动脉内皮细胞（HAEC）中细胞磷脂（PL）释放AA及前列环素分泌的影响。
方法与结果
siRNA介导的ATGL沉默促进了HAEC中脂滴形成和甘油三酯（TG）积累（尼罗红染色）。ATGL基因敲低降低了基础状态下及A23187（钙离子载体）诱导的（用C-AA标记的）HAEC中C-AA的释放。在A23187刺激的ATGL沉默细胞中，这伴随着细胞PL中C-AA含量的降低和前列环素分泌的减少（通过6-酮-PGF1α酶免疫分析测定）。
结论
在血管内皮细胞中，刺激诱导的AA释放和前列环素分泌效率依赖于ATGL。
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