文献简介

出版社:PLOS ONE

作  者:Tao Chen, Zai-pei Guo, Li Li, Meng-meng Li, Ting-ting Wang, Rui-zhen Jia, Na Cao, Jing-yi Li

编  号:10.1371/journal.pone.0056830

关键字:

年  份:2013   点击量:892

文献摘要

Abstract

Our previous work indicated that TWEAK is associated with various types of cutaneous vasculitis (CV). Herein, we investigate the effects of TWEAK on vascular injury and adhesion molecule expression in CV mice. We showed that TWEAK priming in mice induced a local CV. Furthermore, TWEAK priming also increased the extravasation of FITC-BSA, myeloperoxidase activity and the expression of E-selectin and ICAM-1. Conversely, TWEAK blockade ameliorated the LPS-induced vascular damage, leukocyte infiltrates and adhesion molecules expression in LPS-induced CV. In addition, TWEAK treatment of HDMECs up-regulated E-selectin and ICAM-1 expression at both mRNA and protein levels. TWEAK also enhanced the adhesion of PMNs to HDMECs. Finally, western blot data revealed that TWEAK can induce phosphorylation of p38, JNK and ERK in HDMECs. These data suggest that TWEAK acted as an inducer of E-selectin and ICAM-1 expression in CV mice and HDMECs, may contribute to the development of CV.

摘要

我们先前的工作研究表明TWEAK与多种皮肤血管炎(CV)有关。在此,我们探讨在患有CV的小鼠中TWEAK对血管损伤和黏附分子表达的影响。我们发现在小鼠中TWEAK启动效应可以诱导局部皮肤血管炎。此外,TWEAK启动效应也增加了FITC-BSA的外渗,髓过氧化物酶活性以及E-选择素和ICAM-1的表达。相反,在LPS诱导CV中,TWEAK阻塞改善了LPS诱导的血管损害、白细胞浸润和粘附分子的表达。另外,在mRNA和蛋白水平上,TWEAK治疗HDMEC均会导致E-选择素和ICAM-1表达的上调。TWEAK也增强了PMNHDMEC的粘附力。最后,免疫印迹数据显示在HDMEC中,TWEAK能够诱导p38JNKERK的磷酸化作用。这些数据表明,在CV小鼠和HDMEC中,TWEAK充当着E-选择素和ICAM-1表达的诱导剂,并且可能有助于皮肤血管炎的发展。