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人胰岛中Fas表达与细胞凋亡诱导之间的解离。

Dissociation between Fas expression and induction of apoptosis in human islets of Langerhans.

作者信息

Loweth A C, Watts K, McBain S C, Williams G T, Scarpello J H, Morgan N G

机构信息

Cellular Pharmacology Group, School of Life Sciences, Keele University, Staffs, UK.

出版信息

Diabetes Obes Metab. 2000 Jan;2(1):57-60. doi: 10.1046/j.1463-1326.2000.00068.x.

Abstract

There is increasing evidence that inappropriate induction of apoptosis in pancreatic beta-cells may precede the development of type 1 diabetes in animal models and in man. One mechanism by which this has been proposed to occur involves up-regulation of the death receptor Fas on beta-cells, resulting in apoptosis of the Fas-bearing beta-cells upon ligation of the receptor. We have examined this hypothesis in isolated human islets of Langerhans and show that--in contrast to data obtained with rodent beta-cells--expression of Fas per se is not sufficient to allow induction of apoptosis upon addition of agonistic anti-Fas serum.

摘要

越来越多的证据表明,在动物模型和人类中,胰腺β细胞中凋亡的不适当诱导可能先于1型糖尿病的发生。有人提出这种情况发生的一种机制涉及β细胞上死亡受体Fas的上调,导致受体连接后携带Fas的β细胞发生凋亡。我们在分离的人胰岛中检验了这一假说,结果表明——与用啮齿动物β细胞获得的数据相反——Fas本身的表达不足以在加入激动性抗Fas血清后诱导凋亡。

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