Trail interacts redundantly with nitric oxide in rat astrocytes: Potential contribution to neurodegenerative processes
Trail interacts redundantly with nitric oxide in rat astrocytes: Potential contribution to neurodegenerative processes
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DOI：
10.1016/j.jneuroim.2006.09.007
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发表时间：
2007-01-01
影响因子：
3.3
通讯作者：
Bernardini, Renato
中科院分区：
文献类型：
--
作者：
Cantarella, Giuseppina;Lempereur, Laurence;Bernardini, Renato
促凋亡细胞因子TRAIL已显示增强淀粉样蛋白β依赖性神经毒性。本文报道了体外培养的大鼠星形胶质细胞中TRAIL与一氧化氮（NO）的相互作用。大鼠星形胶质细胞表达所有TRAIL受体mRNA和蛋白。然而，TRAIL未能诱导星形胶质细胞凋亡，而这些细胞释放大量的亚硝酸盐。TRAIL中和抗体能够阻止LPS诱导的星形胶质细胞中的iNOS表达。有趣的是，TRAIL诱导其自身在星形胶质细胞中的表达。这些数据表明，星形胶质细胞中TRAIL和NO之间的冗余可能会加剧神经元损伤/死亡过程，可能会发现治疗神经退行性疾病的新分子靶点。(c)2006 Elsevier B. V.保留所有权利。
The proapoptotic cytokine TRAIL has been shown to enhance amyloid-beta-dependent neurotoxicity. Here are reported interactions between TRAIL and nitric oxide (NO) in cultured rat astrocytes in vitro. Rat astrocytes expressed all TRAIL receptor mRNAs and proteins. However, TRAIL failed in inducing apoptosis of astrocytes, whereas these cells released substantial amounts of nitrites. A TRAIL-neutralizing antibody was able to prevent LPS-induced iNOS expression in astrocytes. Interestingly, TRAIL induced its own expression in astrocytes. These data suggest that redundancy between TRAIL and NO in astrocytes could be fueling neuronal damage/death processes, potentially uncovering novel molecular targets for the treatment of neurodegenerative disorders. (c) 2006 Elsevier B.V. All rights reserved.