LncRNA MIR155HG contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-128-5p/BRD4 axis.

Bioscience Reports
Jie SongLiguo Zong

Abstract

Chronic obstructive pulmonary disease (COPD) is a common airway disease characterized by an exaggerated pulmonary inflammatory response. Long noncoding MIR155 host gene (lncRNA MIR155HG) has been identified to be related to the macrophage polarization in COPD. However, the detailed function of MIR155HG in cigarette smoke (CS)-mediated COPD remains largely unknown. The expression level of MIR155HG was elevated while miR-218-5p was decreased in lung tissues of smokers without or with COPD, especially in smokers with COPD, and cigarette smoke extract (CSE)-treated human pulmonary microvascular endothelial cell (HPMECs) in a dose- and time-dependent manner. Then, functional experiments showed that MIR155HG deletion could reverse CSE exposure-induced apoptosis and inflammation in HPMECs. MiR-218-5p was confirmed to be a target of MIR155HG and rescue assay showed miR-218-5p inhibitor attenuated the inhibitory action of MIR155HG knockdown on CSE-induced HPMECs. Subsequently, miR-218-5p was found to target bromodomain containing 4 (BRD4) directly, and miR-218-5p overexpression overturned CSE-induced injury of HPMECs via regulating BRD4. Additionally, co-expression analysis indicated MIR155HG indirectly regulated BRD4 expression in HPME...Continue Reading

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Citations

Jan 20, 2021·Signal Transduction and Targeted Therapy·Nian WangRui Kang
Apr 10, 2021·International Journal of Chronic Obstructive Pulmonary Disease·Zheng WangZhihong Gao
Apr 16, 2021·International Journal of Chronic Obstructive Pulmonary Disease·Caifen ZhengXinying Wang

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Methods Mentioned

BETA
transfection
PCR
flow cytometry
protein assay
immunoprecipitation
RIP
ELISA

Software Mentioned

Image Lab
DianaTools
GraphPad Prism
DIANA

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