Exposure to PM2.5 induces aberrant activation of NF-κB in human airway epithelial cells by downregulating miR-331 expression

Song, Lei; Li, Dan; Li, Xiaoping; Ma, Lu‐Fang; Bai, Xiaoxue; Zhang, Wen; Zhang, Xiufang; Chen, Dong; Peng, Liping

doi:10.1016/j.etap.2017.02.011

Cited by 74 publications

(39 citation statements)

References 28 publications

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“…Beas-2B cells, where its overexpression inhibits the activation of NF-κB and the expression of IL-6 and IL-8 in response to particulate matter (Song et al, 2017). Also, miR-708, which was also downregulated in our model, was proven to have anti-inflammatory roles in endothelial cells isolated from human aorta by inhibiting NF-κB signaling (Chen et al, 2015).…”

Section: Figurementioning

confidence: 63%

“…Thus, in our model this miR also may be responsible of the later increase in Ocn and Runx2 gene expression (Gámez, Rodríguez‐Carballo, Bartrons, Rosa, & Ventura, ). MiR‐331, which was downregulated in our model at day 3, was shown to be anti‐inflammatory in human airway epithelial Beas‐2B cells, where its overexpression inhibits the activation of NF‐κB and the expression of IL‐6 and IL‐8 in response to particulate matter (Song et al, ). Also, miR‐708, which was also downregulated in our model, was proven to have anti‐inflammatory roles in endothelial cells isolated from human aorta by inhibiting NF‐κB signaling (Chen et al, ).…”

Section: Discussionmentioning

confidence: 85%

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Characterization and assessment of potential microRNAs involved in phosphate‐induced aortic calcification

Fakhry

Skafi

Fayyad‐Kazan

et al. 2017

Journal Cellular Physiology

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Medial artery calcification, a hallmark of type 2 diabetes mellitus and chronic kidney disease (CKD), is known as an independent risk factor for cardiovascular mortality and morbidity. Hyperphosphatemia associated with CKD is a strong stimulator of vascular calcification but the molecular mechanisms regulating this process remain not fully understood. We showed that calcification was induced after exposing Sprague-Dawley rat aortic explants to high inorganic phosphate level (P , 6 mM) as examined by Alizarin red and Von Kossa staining. This calcification was associated with high Tissue-Nonspecific Alkaline Phosphatase (TNAP) activity, vascular smooth muscle cells de-differentiation, manifested by downregulation of smooth muscle 22 alpha (SM22α) protein expression which was assessed by immunoblot analysis, immunofluorescence, and trans-differentiation into osteo-chondrocyte-like cells revealed by upregulation of Runt related transcription factor 2 (Runx2), TNAP, osteocalcin, and osteopontin mRNA levels which were determined by quantitative real-time PCR. To unravel the possible mechanism(s) involved in this process, microRNA (miR) expression profile, which was assessed using TLDA technique and thereafter confirmed by individual qRT-PCR, revealed differential expression 10 miRs, five at day 3 and 5 at day 6 post P treatment versus control untreated aortas. At day 3, miR-200c, -155, 322 were upregulated and miR-708 and 331 were downregulated. After 6 days of treatment, miR-328, -546, -301a were upregulated while miR-409 and miR-542 were downregulated. Our results indicate that high P levels trigger aortic calcification and modulation of certain miRs. These observations suggest that mechanisms regulating aortic calcification might involve miRs, which warrant further investigations in future studies.

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Section: Figurementioning

confidence: 63%

Section: Discussionmentioning

confidence: 85%

Characterization and assessment of potential microRNAs involved in phosphate‐induced aortic calcification

Fakhry

Skafi

Fayyad‐Kazan

et al. 2017

Journal Cellular Physiology

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“…Ambient PM/DEPs exposure was further associated with the overexpression of several genes and increased phosphorylated proteins related to the MAPK or PI3K/AKT pathway . Several studies also demonstrated that PM activates NF‐ κB signalling in airway epithelial cells to induce inflammation …”

Section: Air Pollution and The Airway Epitheliummentioning

confidence: 99%

“…More specifically, it was suggested that the suppressive effects of Ahr on NF‐κB's transcriptional activity are down‐regulated by miRNA‐375, leading to increased TSLP expression . Moreover, increased IL‐6 and IL‐8 production upon PM exposure was suggested to depend on a sustained activation of NF‐κB, which was regulated by a ROS/PI3K/AKT‐dependent down‐regulation of miRNA‐331 expression in airway epithelial cells . Notably, mechanistic insights concerning the altered expression of typical type 2‐promoting cytokines, such as IL‐25, IL‐33 and TSLP, towards PM exposure are highly lacking.…”

Section: How Does Particulate Matter Influence Epithelial Cytokine Exmentioning

confidence: 99%

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Insights in particulate matter‐induced allergic airway inflammation: Focus on the epithelium

Grove

Provoost

Brusselle

et al. 2018

Clin Experimental Allergy

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Outdoor air pollution is a major environmental health problem throughout the world. In particular, exposure to particulate matter (PM) has been associated with the development and exacerbation of several respiratory diseases, including asthma. Although the adverse health effects of PM have been demonstrated for many years, the underlying mechanisms have not been fully identified. In this review, we focus on the role of the lung epithelium and specifically highlight multiple cytokines in PM-induced respiratory responses. We describe the available literature on the topic including in vitro studies, findings in humans (ie observations in human cohorts, human controlled exposure and ex vivo studies) and in vivo animal studies. In brief, it has been shown that exposure to PM modulates the airway epithelium and promotes the production of several cytokines, including IL-1, IL-6, IL-8, IL-25, IL-33, TNF-α, TSLP and GM-CSF. Further, we propose that PM-induced type 2-promoting cytokines are important mediators in the acute and aggravating effects of PM on airway inflammation. Targeting these cytokines could therefore be a new approach in the treatment of asthma.

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Fine Particulate Matter Induces Childhood Asthma Attacks via Extracellular Vesicle‐Packaged Let‐7i‐5p‐Mediated Modulation of the MAPK Signaling Pathway

Zheng

Tian

et al. 2021

Advanced Science

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Fine particulate matter less than 2.5 µm in diameter (PM2.5) is a major risk factor for acute asthma attacks in children. However, the biological mechanism underlying this association remains unclear. In the present study, PM2.5‐treated HBE cells‐secreted extracellular vesicles (PM2.5‐EVs) caused cytotoxicity in “horizontal” HBE cells and increased the contractility of “longitudinal” sensitive human bronchial smooth muscle cells (HBSMCs). RNA sequencing showed that let‐7i‐5p is significantly overexpressed in PM2.5‐EVs and asthmatic plasma; additionally, its level is correlated with PM2.5 exposure in children with asthma. The combination of EV‐packaged let‐7i‐5p and the traditional clinical biomarker IgE exhibits the best diagnostic performance (area under the curve [AUC] = 0.855, 95% CI = 0.786–0.923). Mechanistically, let‐7i‐5p is packaged into PM2.5‐EVs by interacting with ELAVL1 and internalized by both “horizontal” recipient HBE cells and “longitudinal” recipient‐sensitive HBSMCs, with subsequent activation of the MAPK signaling pathway via suppression of its target DUSP1. Furthermore, an injection of EV‐packaged let‐7i‐5p into PM2.5‐treated juvenile mice aggravated asthma symptoms. This comprehensive study deciphered the remodeling of the extracellular environment mediated by the secretion of let‐7i‐5p‐enriched EVs during PM2.5‐induced asthma attacks and identified plasma EV‐packaged let‐7i‐5p as a novel predictor of childhood asthma.

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Exposure to PM2.5 induces aberrant activation of NF-κB in human airway epithelial cells by downregulating miR-331 expression

Cited by 74 publications

References 28 publications

Characterization and assessment of potential microRNAs involved in phosphate‐induced aortic calcification

Characterization and assessment of potential microRNAs involved in phosphate‐induced aortic calcification

Insights in particulate matter‐induced allergic airway inflammation: Focus on the epithelium

Fine Particulate Matter Induces Childhood Asthma Attacks via Extracellular Vesicle‐Packaged Let‐7i‐5p‐Mediated Modulation of the MAPK Signaling Pathway

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