Interferon-gamma synergises with tumour necrosis factor and lymphotoxin-alpha to enhance the mRNA and protein expression of adhesion molecules in mouse brain endothelial cells.

Weiser S; Miu J; Ball HJ; Hunt NH

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Interferon-gamma synergises with tumour necrosis factor and lymphotoxin-alpha to enhance the mRNA and protein expression of adhesion molecules in mouse brain endothelial cells.

机译：干扰素-γ与肿瘤坏死因子和淋巴毒素-α协同作用，以增强小鼠脑内皮细胞粘附分子的mRNA和蛋白质表达。

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Changes to the cerebral microvasculature are evident during cerebral malaria (CM). Activation of the endothelium is likely to be due to the actions of cytokines, circulating levels of which are elevated during CM. Endothelial cells are known to up-regulate the expression of cellular adhesion molecules, which can lead to cellular sequestration and obstruction of vessels. However, it is unknown whether cytokines synergise in the up-regulation of the adhesion molecules involved in CM. In this study, the mRNA and/or protein expression of the adhesion molecules vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), P-selectin and E-Selectin were examined in a mouse brain endothelial cell line. Endothelial cells were stimulated with interferon-gamma (IFN-gamma), tumour necrosis factor (TNF) and lymphotoxin-alpha (LT-alpha), alone or in combination. The expression of ICAM-1, VCAM-1, P-selectin and E-Selectin mRNA in mouse brain endothelial cells by TNF and/or LT-alpha was found to be significantly enhanced in the presence of IFN-gamma. The same synergistic effect was found when analyzing ICAM-1 protein expression in cytokine stimulated mouse brain endothelial cells. The findings show that cytokines can synergise to influence gene expression and protein expression in a mouse brain endothelial cell line.

机译：在脑疟疾（CM）期间，脑微血管的变化很明显。内皮的活化可能是由于细胞因子的作用，其循环水平在CM期间升高。已知内皮细胞上调细胞粘附分子的表达，这可能导致细胞螯合和血管阻塞。然而，尚不清楚细胞因子是否在参与CM的粘附分子上调中协同作用。在这项研究中，在小鼠中检查了粘附分子血管细胞粘附分子-1（VCAM-1），细胞间粘附分子-1（ICAM-1），P-选择素和E-选择素的mRNA和/或蛋白质表达脑内皮细胞系。单独或组合用干扰素-γ（IFN-γ），肿瘤坏死因子（TNF）和淋巴毒素-α（LT-α）刺激内皮细胞。发现在IFN-γ的存在下，TNF和/或LT-α在小鼠脑内皮细胞中ICAM-1，VCAM-1，P-选择素和E-选择素mRNA的表达显着增强。分析细胞因子刺激的小鼠脑内皮细胞中的ICAM-1蛋白表达时，发现了相同的协同作用。这些发现表明，细胞因子可以协同作用来影响小鼠脑内皮细胞系中的基因表达和蛋白质表达。

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《Cytokine》 |2007年第1期|共8页
作者
Weiser S; Miu J; Ball HJ; Hunt NH;
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正文语种 eng
中图分类细胞生物学;
关键词
Endothelial cell; Laboratory mice; Brain; lymphotoxin-alpha; 脑;

机译：内皮细胞;实验室小鼠;脑;lymphotoxin-alpha;脑;

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专利

1. Interferon-gamma synergises with tumour necrosis factor and lymphotoxin-alpha to enhance the mRNA and protein expression of adhesion molecules in mouse brain endothelial cells. [J] . Weiser S, Miu J, Ball HJ, Cytokine . 2007,第1期

机译：干扰素-γ与肿瘤坏死因子和淋巴毒素-α协同作用，以增强小鼠脑内皮细胞粘附分子的mRNA和蛋白质表达。
2. Endothelin-1 enhances vascular cell adhesion molecule-1 expression in tumor necrosis factor alpha-stimulated vascular endothelial cells. [J] . Ishizuka T, Takamizawa Matsumoto-M, Suzuki K, European Journal of Pharmacology: An International Journal . 1999,第2期

机译：内皮素-1增强肿瘤坏死因子α刺激的血管内皮细胞中的血管细胞粘附分子1表达。
3. CAMP-response element-binding protein mediates tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 expression in endothelial cells. [J] . Ono H, Ichiki T, Ohtsubo H, Hypertension research: Official journal of the Japanese Society of Hypertension . 2006,第1期

机译：CAMP反应元件结合蛋白介导内皮细胞中肿瘤坏死因子-α诱导的血管细胞粘附分子1表达。
4. Pravastatin and Rosiglitazone May Attenuate Coronary Artery Disease by Decreasing Interferon-gamma, Tumor Necrosis Factor-alpha, Interleukin-6, Macrophage Chemotactic Protein-1, C-Reactive Protein, and Increasing Interleukin-4 [C] . L.G. Tan, S.A. Tan, L.S. Berk International Congress on Coronary Artery Disease . 2007

机译：普伐他汀和罗格列酮可以通过减少干扰素-γ，肿瘤坏死因子-α，白细胞介素-6，巨噬细胞趋化蛋白-1，C反应蛋白和增加白细胞介素-4
5. Expression of the sulfated glucuronyl acid (SGA) epitope and neural cell adhesion molecule (NCAM) in cultured bovine brain microvascular endothelial cells. [D] . Tranduc, Matthew H. 1998

机译：硫酸化的葡萄糖醛酸酸（SGA）表位和神经细胞粘附分子（NCAM）在培养的牛脑微血管内皮细胞中的表达。
6. Reduced Expression of Adipose Triglyceride Lipase Enhances Tumor Necrosis Factor α-induced Intercellular Adhesion Molecule-1 Expression in Human Aortic Endothelial Cells via Protein Kinase C-dependent Activation of Nuclear Factor-κB [O] . Tomoaki Inoue, Kunihisa Kobayashi, Toyoshi Inoguchi, 2011

机译：脂肪甘油三酯脂肪酶表达的减少通过蛋白激酶C依赖性核因子-κB的活化增强了肿瘤坏死因子α诱导的人主动脉内皮细胞中细胞间粘附分子1的表达。
7. Enhanced binding of lymphocytes from patients with multiple sclerosis to tumour necrosis factor-alpha (TNF-α)-treated endothelial monolayers: associations with clinical relapse and adhesion molecule expression [O] . VORA, A J, PERKIN, G D, McCOY, T, 1996

机译：多发性硬化症患者的淋巴细胞与肿瘤坏死因子-α（TNF-α）治疗的内皮细胞单层的结合增强：与临床复发和粘附分子表达的关联

Interferon-gamma synergises with tumour necrosis factor and lymphotoxin-alpha to enhance the mRNA and protein expression of adhesion molecules in mouse brain endothelial cells.

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