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首页> 外文期刊>Human and Experimental Toxicology >MicroRNA-150 protects against cigarette smoke-induced lung inflammation and airway epithelial cell apoptosis through repressing p53: MicroRNA-150 in CS-induced lung inflammation
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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

机译：MicroRNA-150通过压制P53：MicroRNA-150在CS诱导的肺炎中保护烟雾诱导的肺炎和气道上皮细胞凋亡

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摘要

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-B) 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-B activity. Restoration of miR-150 expression may represent a potential therapeutic strategy for CS-related COPD.
机译：香烟烟雾（CS）暴露是慢性阻塞性肺疾病（COPD）的重要危险因素。MicroRNA-150（miR-150）参与多种炎症性疾病。然而，对于miR-150在COPD发病机制中的作用知之甚少。在本研究中，我们建立了CS相关的COPD小鼠模型，并评估了miR-150对CS诱导的肺部炎症的影响。我们进一步研究了miR-150过度表达对暴露于CS提取物（CSE）的气道上皮细胞中促炎性细胞因子产生和凋亡的影响。研究发现，与正常空气条件下的对照组小鼠相比，暴露于CS的小鼠肺中的miR-150显著下调（p；0.05）。与对照细胞相比，暴露于CSE的BEAS-2B气道上皮细胞的miR-150水平降低了四到六倍（p；0.05）。输送miR-150模拟物可减轻CS诱导的肺部炎症，并在支气管肺泡灌洗液中积聚中性粒细胞、淋巴细胞和巨噬细胞。此外，miR-150的过度表达阻止了CSE诱导BEAS-2B细胞中白细胞介素-6、肿瘤坏死因子α和白细胞介素-8的表达以及核因子-κB（NF-B）的转录活性。此外，miR-150保护BEAS-2B细胞免受CSE诱导的凋亡，这与p53表达降低有关。在miR-150过度表达的BEAS-2B细胞中，p53的共同表达恢复了对CSE的凋亡反应。总之，miR-150抑制CS诱导的肺部炎症和气道上皮细胞凋亡，这与抑制p53表达和NF-B活性有关。miR-150表达的恢复可能是CS相关COPD的潜在治疗策略。

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