MicroRNA Profiling Reveals a Role for MicroRNA-218-5p in the Pathogenesis of Chronic Obstructive Pulmonary Disease

Abstract

We highlight a role for miR-218-5p in the pathogenesis of COPD.

Shifting from Correlation to Causation: Challenges for the Future of Unbiased Molecular Studies in Inflammatory Lung Disease

“…43-56) investigate the role of miR-218-5p in the response to tobacco smoke and hypothesize a role for this miRNA in COPD pathogenesis (18). They first show that expression of miR-218-5p is decreased in the lung tissue of smokers, similar to previous studies (11,19,20).…”

MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD

“…COPD patients (10) and healthy nonsmoking (10) and smoking (5) controls were recruited, and their characteristics are shown in Table 1. Subject recruitment, viruses, cell culture and viral infection, A20 plasmid, siRNA, miR-125a and -b antagomir/mimetic treatment, cloning and mutagenesis of miR-125a and -b binding sites in MAVS 3′-UTR, reporter assays, immunoblotting, cytometric bead array, immunoprecipitation, miRNA extraction and analysis, and statistical tests were performed as previously described and/or as in Supplemental Methods (27,31,57,58). In vivo.…”

“…We also showed that primary BECs (pBECs) from COPD subjects and our established in vivo model of experimental COPD have increased inflammatory and impaired antiviral responses to IAV infections, leading to more severe infection (27)(28)(29). Furthermore, miRNAs are known to be altered in COPD (30,31). However, the molecular mechanisms underpinning the heightened inflammatory response in IAV infections and defective immune responses in COPD remain unclear.…”

The role of microRNAs in chronic respiratory disease: recent insights

“…miR135b decreased the expression of interleukin 1 receptor (IL-1R1) through its 3′ UTR and was also a target of signaling through the IL-1 pathway, suggesting this miRNA as a critical regulator of IL-1-mediated neutrophilic inflammation (Halappanavar et al, 2013). Furthermore, miR-218-5p was found to be significantly downregulated in lung tissue of smoke-exposed mice and humans (Conickx et al, 2017).…”