Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke

Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke
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DOI:
10.1016/j.jns.2008.08.005
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发表时间:
2008-12-15
影响因子:
4.4
通讯作者:
Schwaninger, Markus
Schwaninger, Markus
中科院分区:
医学3区
文献类型:
--
作者:
Inta, Ioana;Frauenknecht, Katrin;Schwaninger, Markus

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中风结果由延迟的神经元细胞死亡和水肿形成决定。 TWEAK 是 TNF 超家族的一种细胞因子,其膜受体 Fn14 促进缺血诱导的神经元凋亡和血脑屏障渗漏。 TWEAK 和 Fn14 在实验性中风模型中均上调。在这项研究中,我们调查了 TWEAK 和 Fn14 在中风患者中是否上调。我们通过 ELISA 测量了中风患者和匹配对照受试者中 TWEAK 的血清浓度。通过实时 RT-PCR 和免疫组织化学评估大脑中 Fn14 的表达。 TWEAK 中风患者的血清浓度升高。在尸检样本中,我们发现受体 Fn14 的 mRNA 水平升高,并且 TWEAK mRNA 水平有升高的趋势。在梗塞和梗塞周围组织中,Fn14 的免疫染色增强。这些数据表明,细胞因子 TWEAK 及其膜受体 Fn14 在中风中上调,表明它们有助于中风结果。 (C) 2008 年爱思唯尔 BY。版权所有。
Stroke outcome is determined by delayed neuronal cell death and edema formation. TWEAK, a cytokine of the TNF superfamily, and its membrane receptor Fn14 promote ischemia-induced neuronal apoptosis and leakage of the blood-brain barrier. Both TWEAK and Fn14 are upregulated in experimental stroke models. in this study, we investigated whether TWEAK and Fn14 are upregulated in stroke patients. We measured serum concentrations of TWEAK in stroke patients and matched control subjects by ELISA. Expression of Fn14 in the brain was evaluated by real-time RT-PCR and immunohistochemistry. TWEAK serum concentrations were elevated in stroke patients. In autopsy samples, we found elevated mRNA levels of the receptor Fn14 and a trend towards higher TWEAK mRNA levels. In the infarcted and peri-infarct tissue immunostaining for Fn14 was enhanced. These data show that the cytokine TWEAK and its membrane receptor Fn14 are upregulated in stroke and suggest that they contribute to stroke outcome. (C) 2008 Elsevier BY. All rights reserved.