MiR‐221‐3p and miR‐92a‐3p enhances smoking‐induced inflammation in COPD. Issue 7 (7th June 2021)

• Record Type: Journal Article
• Authors: Shen, Yahui; Lu, Huiyu; Song, Guixian
• Is Part Of: Journal of clinical laboratory analysis. Volume 35:Issue 7(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-06-07
• Subjects: chronic obstructive pulmonary disease -- cigarette smoke extract -- diagnosis -- inflammation -- miR‐221‐3p -- miR‐92a‐3p; Diagnosis, Laboratory -- Periodicals; Medical laboratory technology -- Periodicals; 616
• DOI: 10.1002/jcla.23857
• Languages: English
• ISSNs: 0887-8013

Abstract

Abstract: Background: Smoking is likely to facilitate airway inflammation and finally contributes to chronic obstructive pulmonary disease (COPD). This investigation was intended to elucidate miRNAs that were involved in smoking‐induced COPD. Methods: Altogether 155 COPD patients and 77 healthy volunteers were recruited, and their serum levels of miR‐221‐3p and miR‐92a‐3p were determined. Besides, human bronchial epithelial cells (16HBECs) were purchased, and they were treated by varying concentrations of cigarette smoke extract (CSE). The 16HBECs were, additionally, transfected by miR‐221‐3p mimic, miR‐92a‐3p mimic, miR‐221‐3p inhibitor or miR‐92a‐3p inhibitor, and cytokines released by them, including TNF‐α, IL‐8, IL‐1β, and TGF‐β1, were monitored using enzyme linked immunosorbent assay (ELISA) kits. Results: Chronic obstructive pulmonary disease patients possessed higher serum levels of miR‐221‐3p and miR‐92a‐3p than healthy volunteers ( p < 0.05), and both miR‐221‐3p and miR‐92a‐3p were effective biomarkers in diagnosing stable COPD from acute exacerbation COPD. Moreover, viability of 16HBECs was undermined by CSE treatment ( p < 0.05), and exposure to CSE facilitated 16HBECs' release of TNF‐α, IL‐8, IL‐1β, and TGF‐β1 ( p < 0.05). Furthermore, miR‐221‐3p/miR‐92a‐3p expression in 16HBECs was significantly suppressed after transfection of miR‐221‐3p/miR‐92a‐3p inhibitor ( p < 0.05), which abated CSE‐triggered increase in cytokine production and decline in viability of 16HBECs ( p < 0.05). Conclusion: MiR‐221‐3p and miR‐92a‐3p were involved in CSE‐induced hyperinflammation of COPD, suggesting that they were favorable alternatives in diagnosing COPD patients with smoking history. Abstract : Serum level of miR‐221‐3p and miR‐92a‐3p was both significantly higher in COPD group than in healthy volunteers. Inhibitors of miR‐221‐3p or miR‐92a‐3p reversed the effects of CSE on 16HBEC viability and apoptosis. Moreover, miR‐221‐3p/miR‐92a‐3p inhibitor also rescued the influence of CSE on inflammatory factors and airway remodeling‐related proteins.