NLRP3 inflammasome inhibition attenuates silica-induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells

Li, Xiang; Yan, Xiaopei; Wang, Yanli; Wang, Jingjing; Zhou, Fang; Wang, Hong; Xie, Weiping; Kong, Hui

doi:10.1016/j.yexcr.2017.12.013

Cited by 52 publications

(31 citation statements)

References 38 publications

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“…For the initiation of the NLRP3 inflammasome, lipopolysaccharide (LPS) is widely considered to be a classic ligand for the activation of the TLR4 ( Chu et al, 2018 ; Ho and Chang, 2018 ). In addition, several factors have been shown to be effective to induce the second step of the NLRP3 inflammasome activation, including the adenosine triphosphate (ATP, triggering the intracellular K + efflux), PAMPs, DAMPs, silica, β-amyloid, autophagy deficiency as well as factors leading to the enhancement of mitochondrial Ca 2+ overload and so on ( Shao et al, 2017b ; Chen et al, 2018 ; Li et al, 2018b ; Meng et al, 2018 ; Zhao et al, 2018 ).…”

Section: Nlrp3 Inflammasomementioning

confidence: 99%

Targeting NLRP3 Inflammasome in the Treatment of CNS Diseases

Shao

Cao

2018

Front. Mol. Neurosci.

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Central nervous system (CNS) is one of the largest killers of people’s health all over the world. The overactivation of the immune and inflammatory responses is considered as an important factor, contributing to the pathogenesis and progression of CNS disorders. Among all kinds of immune and inflammatory reaction, the inflammasome, a complex of proteins, has been drawn increasingly attention to by researchers. The initiation and activation of the inflammasome is involved in the onset of various kinds of diseases. The NLRP3 inflammasome, the most studied member of the inflammasome, is closely associated with many kinds of CNS disorders. Here in this review, the roles of the NLRP3 inflammasome in the pathogenesis and progression of several well-known CNS diseases would be discussed, including cerebrovascular diseases, neurodegenerative diseases, multiple sclerosis, depression as well as other CNS disorders. In addition, several therapeutic strategies targeting on the NLRP3 inflammasome for the treatment of CNS disorders would be described in this review.

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Section: Nlrp3 Inflammasomementioning

confidence: 99%

Targeting NLRP3 Inflammasome in the Treatment of CNS Diseases

Shao

Cao

2018

Front. Mol. Neurosci.

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“…Several prior studies used A549 as an in vitro model to study lung cancer [ 22–24 ], However, we used normal bronchial epithelial cells 16HBE in our study. EMT in 16HBE cells can be induced by silicon dioxide [ 25 ], smoking extract (CSE) [ 26 ], and transforming growth factor β1 (TGF-β1) [ 27–29 ]. The novelty of the present study was in the use of the 16HBE cells and the induction of EMT using ionizing radiation.…”

Section: Discussionmentioning

confidence: 99%

Ionizing radiation induces epithelial–mesenchymal transition in human bronchial epithelial cells

Tang

Cui

et al. 2020

Bioscience Reports

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Objective: This study aimed to analyze the mechanism by which long-term occupational exposure of workers to low-dose ionizing irradiation induces epithelial mesenchymal transition (EMT) of the human bronchial epithelial cells using transcriptome profiling.Methods: RNA-seq transcriptomics was used to determine gene expression in blood samples from radiation-exposed workers followed by bioinformatics analysis. Normal bronchial epithelial cells (16HBE) were irradiated for different durations and subjected to immunofluorescence, western blotting, scratch healing, and adhesion assays to detect the progression of EMT and its underlying molecular mechanisms.Results: Transcriptomics revealed that exposure to ionizing radiation led to changes in the expression of genes related to EMT, immune response, and migration. At increased cumulative doses, ionizing radiation-induced significant EMT, as evidenced by a gradual decrease in the expression of E-cadherin, increased vimentin, elevated migration ability, and decreased adhesion capability of 16HBE cells. The expression of fibronectin 1 (FN1) showed a gradual increase with the progression of EMT, and may be involved in EMT.Conclusion: Ionizing radiation induces EMT. FN1 may be involved in the progression of EMT and could serve as a potential biomarker for this process.

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“…However, some improvement for pirfenidone and nintedanib might also be found in silicosis. In in vitro measurement, pirfenidone added to human bronchial epithelial cells suppressed silica-induced epithelialmesenchymal transition (EMT) and activation of NLRP3 inflammasome [88]. In rats, pirfenidone reduced silica-induced inflammation and alveolar damage; decreased levels of TNFα, IL-1β and IL-6 in the lung tissue; decreased the expression of collagen I and vimentin; and suppressed the expression of TGFβ1, Smad2/3 and EMT [89].…”

Section: Anti-fibrotic Drugsmentioning

confidence: 99%

New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis

Adamcakova

Mokrá

2021

IJMS

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Inhalation of silica particles is an environmental and occupational cause of silicosis, a type of pneumoconiosis. Development of the lung silicosis is a unique process in which the vicious cycle of ingestion of inhaled silica particles by alveolar macrophages and their release triggers inflammation, generation of nodular lesions, and irreversible fibrosis. The pathophysiology of silicosis is complex, and interactions between the pathomechanisms have not been completely understood. However, elucidation of silica-induced inflammation cascades and inflammation-fibrosis relations has uncovered several novel possibilities of therapeutic targeting. This article reviews new information on the pathophysiology of silicosis and points out several promising treatment approaches targeting silicosis-related pathways.

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NLRP3 inflammasome inhibition attenuates silica-induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells

Cited by 52 publications

References 38 publications

Targeting NLRP3 Inflammasome in the Treatment of CNS Diseases

Targeting NLRP3 Inflammasome in the Treatment of CNS Diseases

Ionizing radiation induces epithelial–mesenchymal transition in human bronchial epithelial cells

New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis

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