MicroRNA-150 protects against cigarette smoke-induced lung inflammation and airway epithelial cell apoptosis through repressing p53: MicroRNA-150 in CS-induced lung inflammation

Dec 6, 2017Human & experimental toxicology

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

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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.

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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 protects against cigarette smoke-induced lung inflammation and airway epithelial cell apoptosis through repressing p53: MicroRNA-150 in CS-induced lung inflammation

Abstract

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