MiR-212-5p exerts a protective effect in chronic obstructive pulmonary disease.

Abstract

Chronic obstructive pulmonary disease (COPD) is a common respiratory tract disease with an incompletely understood pathogenesis. According to previous reports, miRNAs play a crucial pathophysiological role in COPD. MiR-212 was reported to be downregulated in COPD patients; however, the role of miR-212 in COPD remains unknown. In this study, the expression level of miR-212-5p and miR-223 decreased significantly in COPD patients compared to healthy controls. In vitro experiments showed that cigarette smoke extract (CSE) induced NCI-H292 cell apoptosis and inhibited cell proliferation. Inflammation and COPD related genes were also upregulated by CSE, while miR-212-5p inhibited the overexpression of these genes. Furthermore, miR-212-5p promoted cell proliferation and inhibited IGFBP3 expression which was induced by CSE. The expression of p-Akt was also inhibited by CSE, while miR-212-5p significantly promoted the phosphorylation of Akt. In summary, our data suggest that miR-212-5p exerts a protective effect in COPD, and may serve as a prognostic biomarker and potential therapeutic target for COPD.

• Authors: Qin Jia, Jing Chang, Qing Hong, Jing-Jian Zhang, Hai Zhou, Feng-Hua Chen
• Journal: Discovery medicine (Discov Med) Vol. 26 Issue 144 Pg. 173-183 (11 2018) ISSN: 1944-7930 [Electronic] United States
• PMID: 30695677 (Publication Type: Journal Article)

Chemical References

• Biomarkers
• MIRN212 microRNA, human
• MicroRNAs

Topics

• Apoptosis (genetics)
• Biomarkers (analysis)
• Case-Control Studies
• Cells, Cultured
• Cytoprotection (genetics)
• Gene Expression Profiling
• Humans
• Lung (metabolism, pathology)
• MicroRNAs (physiology)
• Molecular Targeted Therapy
• Pulmonary Disease, Chronic Obstructive (genetics, metabolism, pathology)