Journal of clinical laboratory analysis · 2021
MiR-221-3p and miR-92a-3p enhances smoking-induced inflammation in COPD.
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Shen Yahui, Lu Huiyu, Song Guixian
Аннотация
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.
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.