Microarray analysis of lung long non-coding RNAs in cigarette smoke-exposed mouse model
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Hao Wang1,*, Lei Chen1,*, Diandian Li1,*, Ni Zeng1, Yanqiu Wu1, Tao Wang1, Yongchun Shen1, Dan Xu1 and Fuqiang Wen1
1Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, and Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu 610041, China
*These authors have contributed equally to this work
Yongchun Shen, email: email@example.com
Fuqiang Wen, email: firstname.lastname@example.org
Keywords: long non-coding RNAs; cigarette smoke; airway inflammation; mice; microarray analysis
Received: September 08, 2017 Accepted: December 05, 2017 Published: December 18, 2017
Several studies have demonstrated the function of long non-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.
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