Long non-coding RNA expression patterns in lung tissues of chronic cigarette smoke induced COPD mouse model
AffiliationUniv Arizona, Div Translat & Regenerat Med
MetadataShow full item record
PublisherNATURE PUBLISHING GROUP
CitationZhang, H., Sun, D., Li, D., Zheng, Z., Xu, J., Liang, X., ... & Lu, W. (2018). Long non-coding RNA expression patterns in lung tissues of chronic cigarette smoke induced COPD mouse model. Scientific reports, 8(1), 7609, https://doi.org/10.1038/s41598-018-25702-3
Rights© The Author(s) 2018. Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at email@example.com.
AbstractLong non-coding RNAs (lncRNAs) have critical regulatory roles in protein-coding gene expression. Aberrant expression profiles of lncRNAs have been observed in various human diseases. In this study, we investigated transcriptome profiles in lung tissues of chronic cigarette smoke (CS)-induced COPD mouse model. We found that 109 lncRNAs and 260 mRNAs were significantly differential expressed in lungs of chronic CS-induced COPD mouse model compared with control animals. GO and KEGG analyses indicated that differentially expressed lncRNAs associated protein-coding genes were mainly involved in protein processing of endoplasmic reticulum pathway, and taurine and hypotaurine metabolism pathway. The combination of high throughput data analysis and the results of qRT-PCR validation in lungs of chronic CS-induced COPD mouse model, 16HBE cells with CSE treatment and PBMC from patients with COPD revealed that NR_102714 and its associated protein-coding gene UCHL1 might be involved in the development of COPD both in mouse and human. In conclusion, our study demonstrated that aberrant expression profiles of lncRNAs and mRNAs existed in lungs of chronic CS-induced COPD mouse model. From animal models perspective, these results might provide further clues to investigate biological functions of lncRNAs and their potential target protein-coding genes in the pathogenesis of COPD.
NoteOpen access journal.
VersionFinal published version
SponsorsNational Key R&D Program of China [2016YFC0903700]; National Natural Science Foundation of China [81520108001, 81220108001, 81770043]; 973 Key Scheme of China [2015CB553406]; Guangzhou Science and Technology Programs for Science Study ; Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme; Guangzhou Department of Science and Technology programs ; Guangzhou Department of Education grant 
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