TAT-BH4 counteracts Aβ toxicity on capillary endothelium
TAT-BH4 counteracts Aβ toxicity on capillary endothelium
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DOI：
10.1016/j.febslet.2007.01.037
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发表时间：
2007-02-20
期刊：
影响因子：
3.5
通讯作者：
Donnini, S.
中科院分区：
文献类型：
--
作者：
Cantara, S.;Thorpe, P. E.;Donnini, S.
氧化应激是导致血脑屏障退化的因素之一。这种现象在诸如阿尔茨海默氏病或脑淀粉样血管病的病理状况期间观察到，其中脑出血非常频繁。这两种疾病的特征是β淀粉样肽沉积在神经元或血管中。氧化应激导致线粒体功能受损和半胱天冬酶激活后的凋亡性细胞死亡。在本文中，我们证明了Bc 1-x1的BH 4结构域作为与达特肽的缀合形式给予内皮细胞，通过激活Akt/内皮型一氧化氮合酶依赖的存活程序来逆转A β诱导的凋亡性细胞死亡。(c)2007年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
Oxidative stress is one of the factor contributing to blood brain barrier degeneration. This phenomenon is observed during pathological conditions such as Alzheimer's disease or cerebral amyloid angiopathy in which brain haemorrhages are very frequent. Both diseases are characterized by beta amyloid peptide deposition either in neurons or in vessels. Oxidative stress leads to impairment of mitochondrial functions and apoptotic cell death subsequent to caspases activation. In this paper we demonstrate that BH4 domain of Bc1-x1 administrated to endothelial cells as the conjugated form with TAT peptide, reverts A beta-induced apoptotic cell death by activating a survival programme which is Akt/endothelial nitric oxide synthase dependent. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.