Microarray analysis of lung long non-coding RNAs in cigarette smoke-exposed mouse model.

Hao Wang,Yanqiu Wu,Diandian Li,Dan Xu,Tao Wang,Lei Chen,Ni Zeng,Yongchun Shen,Fuqiang Wen

doi:10.18632/oncotarget.23362

Abstract

Several studies have demonstrated the function of long nonâ€‘coding RNAs (lncRNAs) in various biological processes, yet their role underlying the susceptibility to cigarette smoke (CS)-induced airway inflammation remains limited. In the present study, we aimed to profile the expression of lncRNAs and mRNAs in CS-exposed mice. C57BL/6 mice were assigned into a single cigarette-smoking machine with or without CS exposure for 4 weeks, followed by lung tissue harvest and RNA isolation. Microarray analysis identified 108 lncRNAs and 119 mRNAs with differential expression levels in CS-exposed mouse lung tissue compared with those in control mice. The expression patterns of several lncRNAs were further confirmed by qRT-PCR. GO and pathway analyses showed that the altered mRNAs were mainly related to the processes of immune response, defense response and cell chemotaxis, cytokine-cytokine receptor interaction and chemokine signaling pathway. Moreover, a single lncRNA may co-expressed with several mRNAs, and so was the mRNA. Our findings uncovered the expression profile of lncRNAs and mRNAs in the lungs of CS-exposed mice, which may offer new insights into pathogenesis of CS-associated airway inflammatory disorders.

Highlights

Tobacco use, primarily associated with cigarette smoking, is a worldwide risk factor of public health
Several studies have demonstrated the function of long non‐coding RNAs in various biological processes, yet their role underlying the susceptibility to cigarette smoke (CS)-induced airway inflammation remains limited
The top 20 differentially expressed long non‐coding RNAs (lncRNAs) and mRNAs identified by microarray analysis are listed in Tables 1 and 2, respectively

Summary

Introduction

Primarily associated with cigarette smoking, is a worldwide risk factor of public health. Cigarette smoke (CS) contains over 7000 toxicants, most of which are etiological factors in the development of inflammatory pulmonary diseases. Chronic CS exposure causes damage to lung resident cells such as airway epitheliums, leading to the release of pro-inflammatory cytokines and the recruit of neutrophils, contributing to airway remodeling and subsequent airflow limitation which has been identified as the prominent feature of chronic obstructive pulmonary disease (COPD) or other CS-related airway inflammatory disorders [1, 2]. Previous studies found that neutrophilic airway inflammation already occurred upon shortterm CS exposure in susceptible mice and humans [3, 4], indicating that genetic or epigenetic factors may play a role in the susceptibility to CS-induced airway inflammation. Several studies demonstrated the function of lncRNAs in the development of pulmonary disorders related to CS. In human bronchial epithelial cells (HBEs), the lncRNA, www.impactjournals.com/oncotarget

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