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Long noncoding RNA atlas of the inflammation caused by asthma in mice

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Abstract

There is little evidence regarding the roles of long noncoding RNAs (lncRNAs) in inflammation caused by asthma. In this study, we successfully generated an asthma mouse model that was induced by ovalbumin (OVA). The effects of dexamethasone (Dex) treatment on lung tissue were investigated using pathological and biochemical methods, including Diff-Quik staining, enzyme-linked immunosorbent assay (ELISA), hematoxylin–eosin (H&E) staining, and western blotting (WB). The inflammation was effectively relieved with Dex treatment. High-throughput sequencing revealed that a total of 1490 lncRNAs were detected in lung tissue samples. Differential expression analysis revealed that the Dex group had 20 upregulated and 15 downregulated lncRNAs compared with those in the Model group. Moreover, nine differentially expressed and inflammation-related lncRNAs were verified by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Furthermore, the regulation networks of these nine lncRNAs, their potential binding microRNA (miRNAs), and the putative target genes showed that these lncRNAs play important roles in the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway. We further identified the expression levels of three potential binding miRNAs by qRT-PCR. The results of this study contribute to a better understanding of the functions of lncRNAs in inflammation caused by asthma.

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Funding

This study was supported by Subitem Fund for Education (Public Hygiene) of Science & Technology Fund Project the Technological Invention and Creative Design Program of the Shenzhen Nanshan District (No. 2019018).

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Correspondence to Feng Xu.

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All authors declare no conflicts of interest.

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The study was approved by the ethics committee of Shenzhen Nanshan People's Hospital.

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Chen, Y., He, Sd., Li, Xd. et al. Long noncoding RNA atlas of the inflammation caused by asthma in mice. Arch. Pharm. Res. 43, 421–432 (2020). https://doi.org/10.1007/s12272-020-01223-4

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  • DOI: https://doi.org/10.1007/s12272-020-01223-4

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