Human & experimental toxicologyDec 6, 2017

MicroRNA-150 may reduce lung inflammation and airway cell death caused by cigarette smoke by lowering p53 levels

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 4, 2026

Abstract

MicroRNA-150 was significantly downregulated in the lungs of cigarette smoke-exposed mice (p < 0.05).

Cigarette smoke exposure is linked to chronic obstructive pulmonary disease (COPD).
A four- to six-fold reduction in miR-150 levels was observed in airway epithelial cells exposed to cigarette smoke extract (CSE) (p < 0.05).
Delivery of miR-150 mimic reduced lung inflammation and immune cell accumulation in bronchoalveolar lavage fluid.
Overexpression of miR-150 inhibited the production of pro-inflammatory cytokines and reduced NF-κB activity in airway epithelial cells exposed to CSE.
MiR-150 overexpression protected airway epithelial cells from apoptosis, which was associated with decreased p53 expression.

Simplified

Cigarette smoke (CS) exposure is an important risk factor for chronic obstructive pulmonary disease (COPD). MicroRNA-150 (miR-150) is involved in several inflammatory diseases. However, little is known about the role of miR-150 in the pathogenesis of COPD. In this study, we established a CS-related mouse model of COPD and evaluated the impact of miR-150 on CS-induced lung inflammation. We further investigated the effects of miR-150 overexpression on pro-inflammatory cytokine production and apoptosis in airway epithelial cells exposed to CS extract (CSE). It was found that miR-150 was significantly ( p < 0.05) downregulated in the lungs of CS-exposed mice, compared to control mice under normal air. The CSE-exposed BEAS-2B airway epithelial cells displayed a four- to six-fold reduction in miR-150 levels, compared to control cells ( p < 0.05). Delivery of miR-150 mimic attenuated CS-induced lung inflammation and accumulation of neutrophils, lymphocytes, and macrophages in bronchoalveolar lavage fluid. Moreover, miR-150 overexpression prevented the induction of interleukin-6, tumor necrosis factor alpha, and interleukin-8 expression and nuclear factor kappa B (NF-κB) transcriptional activity in BEAS-2B cells by CSE. Additionally, miR-150 protected BEAS-2B cells from CSE-induced apoptosis, which was associated with reduced p53 expression. Co-expression of p53 restored apoptotic response to CSE in miR-150-overexpressing BEAS-2B cells. Collectively, miR-150 suppresses CS-induced lung inflammation and airway epithelial cell apoptosis, which is causally linked to repression of p53 expression and NF-κB activity. Restoration of miR-150 expression may represent a potential therapeutic strategy for CS-related COPD.

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MicroRNA-150 may reduce lung inflammation and airway cell death caused by cigarette smoke by lowering p53 levels

Abstract

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