Expression of ADAM-17, TIMP-3 and fractalkine in the human adult brain endothelial cell line, hCMEC/D3, following pro-inflammatory cytokine treatment

Expression of ADAM-17, TIMP-3 and fractalkine in the human adult brain endothelial cell line, hCMEC/D3, following pro-inflammatory cytokine treatment
复制标题

DOI:
10.1016/j.jneuroim.2009.02.008
复制
发表时间:
2009-05-29
影响因子:
3.3
通讯作者:
Woodroofe, M. Nicola
Woodroofe, M. Nicola
中科院分区:
医学4区
文献类型:
--
作者:
Hurst, Louise A.;Bunning, Rowena A. D.;Woodroofe, M. Nicola

文献摘要

被引文献

相似文献

ADAM-17的表达定位于人类中枢神经系统(CNS)的内皮细胞,并在多发性硬化症(MS)白质中增加,提示其在MS发病机制中起作用。研究了促炎细胞因子在人脑内皮细胞株(hCMEC/D3)中的表达情况。肿瘤坏死因子(TNF)显著增加fractalkine mRNA(> 100倍)和蛋白表达,这与fractalkine从细胞中脱落增加有关。Fractalkine的脱落可能调节免疫细胞向中枢神经系统的运输,然而,这似乎不是由ADAM-17活性直接控制的。(C) 2009 Elsevier B.V.版权所有
ADAM-17 expression is localised to endothelial cells in the human central nervous system (CNS) and is increased in multiple sclerosis (MS) white matter, suggesting a role in MS pathogenesis. Expression of ADAM-17, TIMP-3, and fractalkine were investigated in a human brain endothelial cell line (hCMEC/D3) after pro-inflammatory cytokine treatment. Tumour necrosis factor (TNF) significantly increased fractalkine mRNA (> 100 fold) and protein expression, which was associated with increased shedding of fractalkine from the cell. Fractalkine shedding may regulate immune cell trafficking into the CNS, however, this does not appear to be directly controlled by ADAM-17 activity. (C) 2009 Elsevier B.V. All rights reserved.