The AMP-activated protein kinase prevents ceramide synthesis de novo and apoptosis in astrocytes
The AMP-activated protein kinase prevents ceramide synthesis de novo and apoptosis in astrocytes
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DOI：
10.1016/s0014-5793(01)02089-0
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发表时间：
2001-02-02
期刊：
影响因子：
3.5
通讯作者：
Guzmán, M
中科院分区：
文献类型：
--
作者：
Blázquez, C;Geelen, MJH;Guzmán, M
脂肪酸通过促进神经酰胺的合成诱导原代星形胶质细胞的凋亡，在该模型中研究了AR IP激活的蛋白激酶(AMPK)在调控细胞凋亡中的可能作用。5-氨基咪唑-4-甲酰胺核糖核苷(AICAR)长期刺激AMPK可阻止细胞凋亡，AICAR钝化脂肪酸诱导的丝氨酸棕榈酰转移酶和神经酰胺合成，而不影响脂肪酸的合成和氧化。AICAR抑制神经酰胺的积累导致选择性地介导脂肪酸诱导的细胞凋亡的Raf-1/细胞外信号调节激酶级联通路的阻断，数据表明AMPK可能对应激刺激诱导的细胞凋亡具有保护作用。(C)2001年欧洲生物化学学会联合会。爱思唯尔科学公司出版。版权所有。
Fatty acids induce apoptosis in primary astrocytes by enhancing ceramide synthesis de novo, The possible role of the AR IP-activated protein kinase (AMPK) in the control of apoptosis was studied in this model. Long-term stimulation of AMPK with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) prevented apoptosis, AICAR blunted fatty acid-mediated induction of serine palmitoyltransferase and ceramide synthesis de novo, without affecting fatty acid synthesis and oxidation. Prevention of ceramide accumulation by AICAR led to a concomitant blockade of the Raf-1/extracellular signal-regulated kinase cascade, which selectively mediates fatty acid-induced apoptosis, Data indicate that AMPK may protect cells from apoptosis induced by stress stimuli. (C) 2001 Federation of European Bicohemical Societies. Published by Elsevier Science B.V. All rights reserved.