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Oncotarget. 2017 Dec 18;8(70):115647-115656. doi: 10.18632/oncotarget.23362. eCollection 2017 Dec 29.

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

Author information

1
Department 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.
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Contributed equally

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.

KEYWORDS:

airway inflammation; cigarette smoke; long non-coding RNAs; mice; microarray analysis

Conflict of interest statement

CONFLICTS OF INTEREST None of the authors has any conflicts of interest related to this article.

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