Xiang Yang, Zhou Xiao-Yan, Tan Yu-Rong, Tan Mei-Ling, Liu Hui-Jun, Liu Chi, Qu Xiang-Ping, Qin Xiao-Qun
Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, PR China.
PLoS One. 2014 Apr 16;9(4):e95533. doi: 10.1371/journal.pone.0095533. eCollection 2014.
Accumulated research has suggested the importance of the adhesion molecules modulation as therapeutic approach for bronchial asthma. Adhesion molecules expression alteration contributes to the pathogenesis of asthma. In order to probe the roles of expression imbalance of adhesion molecules in asthma pathogenesis, expression profiling of adhesion molecules was performed using cDNA microarray assay. The results showed that the expression pattern of adhesion molecules was altered in peripheral blood leucocytes of asthma patients. In this study, we focused on one of the abnormally expressed molecule, integrin β4, which was down-regulated in all asthma patients, to analyze the relevance of asthma susceptibility with the alteration of integrin β4 expressions. Real time PCR was used to verify the down-regulation of integrin β4 in additional 38 asthma patients. Next, the 5'flanking region of integrin β4 DNA were amplified, sequenced and site-directed mutagenesis technology in correspondent variation sites were carried out. Among 4 variation sites found in 5' flanking region of integrin β4, 3 were related to asthma susceptibility: -nt1029 G/A, -nt 1051 G/A, and -nt 1164 G/C. A reduction of human integrin β4 promoter activity was observed at mutants of these sites. This study demonstrates that various adhesion molecules in asthma patients are abnormally expressed. Mutations in 5' flanking region result in reduced integrin β4 expression, which is related to increased risk of asthma.
积累的研究表明,调节黏附分子作为支气管哮喘的治疗方法具有重要意义。黏附分子表达的改变有助于哮喘的发病机制。为了探究黏附分子表达失衡在哮喘发病机制中的作用,使用cDNA微阵列分析对黏附分子进行表达谱分析。结果显示,哮喘患者外周血白细胞中黏附分子的表达模式发生了改变。在本研究中,我们聚焦于其中一种异常表达的分子整合素β4,它在所有哮喘患者中均下调,以分析整合素β4表达改变与哮喘易感性的相关性。使用实时PCR在另外38例哮喘患者中验证整合素β4的下调。接下来,扩增整合素β4 DNA的5'侧翼区域,进行测序并在相应变异位点进行定点诱变技术。在整合素β4的5'侧翼区域发现的4个变异位点中,3个与哮喘易感性相关:-nt1029 G/A、-nt 1051 G/A和-nt 1164 G/C。在这些位点的突变体中观察到人类整合素β4启动子活性降低。本研究表明,哮喘患者中的各种黏附分子表达异常。5'侧翼区域的突变导致整合素β4表达降低,这与哮喘风险增加有关。