Up-regulation of integrin β3 expression in porcine vascular endothelial cells cultured in vitro by classical swine fever virus
Up-regulation of integrin β3 expression in porcine vascular endothelial cells cultured in vitro by classical swine fever virus
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DOI：
10.1016/j.vetimm.2009.07.005
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发表时间：
2010-02-15
影响因子：
1.8
通讯作者：
Sun, Pei
中科院分区：
文献类型：
--
作者：
Tang, Qing-hai;Zhang, Yan-ming;Sun, Pei
猪瘟（Classical Swine Fever，CSF）是由猪瘟病毒（Classical Swine Fever Virus，CSFV）强毒株引起的一种以弥散性血管内凝血、血小板减少和免疫抑制为特征的猪出血性疾病。细胞粘附分子，整合素β 3，在维持和调节血管通透性中起核心作用。鉴于该疾病的出血病理学，使用猪脐静脉内皮细胞（SUVEC）系结合定量PCR和Western印迹技术研究CSFV感染对整合素β 3表达的影响。感染后，整合素β 3的表达水平与相应的转录水平一起沿着显著上调。感染的内皮细胞粘附到固定化的细胞外基质（ECM）上，比对照更广泛地扩散，并且这种相互作用被抗整合素β 3单克隆抗体（mAb）强烈抑制。提示CSFV感染后血管内皮细胞整合素β 3表达上调，这种细胞粘附分子可能在CSF出血病理过程中止血平衡的改变中起重要作用。皇冠版权所有（C）2009年出版的爱思唯尔B.V.保留所有权利。
Classical swine fever (CSF) caused by virulent strains of classical swine fever virus (CSFV) is a haemorrhagic disease of pigs, characterized by disseminated intravascular coagulation, thrombocytopenia and immunosuppression. The cell adhesion molecule, integrin beta 3, plays a central role in maintaining and regulating vascular permeability. In view of the haemorrhagic pathology of the disease, the effect of CSFV infection on integrin beta 3 expression was investigated using the swine umbilical vein endothelial cell (SUVEC) line, in conjunction with quantitative PCR and Western blotting techniques. Following infection, the expression levels of integrin beta 3 were significantly up-regulated along with corresponding transcription levels. The infected endothelial cells adhered onto immobilized extracellular matrix (ECM) with more extensive spreading than that of the control, and such interaction was strongly inhibited by an anti-integrin beta 3 monoclonal antibody (mAb). This study revealed the up-regulation of integrin beta 3 in vascular endothelial cells by CSFV infection, and cell adhesion molecules of this kind possibly play an important role in the changes of haemostatic balance in haemorrhagic pathology of CSF. Crown Copyright (C) 2009 Published by Elsevier B.V. All rights reserved.