Deducting MicroRNA-Mediated Changes Common in Bronchial Epithelial Cells of Asthma and Chronic Obstructive Pulmonary Disease—A Next-Generation Sequencing-Guided Bioinformatic Approach

Tsai, Ming‐Ju; Tsai, Yu-Chen; Chang, Wei‐An; Lin, Yi-Shiuan; Tsai, Pei-Hsun; Sheu, Chau‐Chyun; Kuo, Po‐Lin; Hsu, Ya‐Ling

doi:10.3390/ijms20030553

Cited by 38 publications

(42 citation statements)

References 67 publications

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“…It is particularly worth noting that the decreased expression of E2F1 in asthma patients is consistent with what we have previously observed in COPD patients [18]. However, it is different from the expression of E2F1 in the lung tissue of lung cancer patients [60]. One possible reason is the speci city of the sample tissue and pathogenic genes.…”

Section: Discussionsupporting

confidence: 87%

“…Although ATG3 is a key molecule that inducing autophagy damage during aging [57], and NUF2 is a gene closely related to aging of lung cells [58], their speci c role in asthma has rarely been studied. The differential expression of ATG3, FOXO3, NUF2 and TP53 in asthma patients were also aligned with former studies [32,[58][59][60]. In addition, excessive secretion of AREG in the airway after an acute attack of asthma promote airway remodeling [56].…”

Section: Discussionsupporting

confidence: 78%

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Variable Expressed Methylation Sites of Aging-related Genes in Asthma

Yang¹,

Lin²,

Yang³

et al. 2020

Preprint

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Background: Asthma is a complex pulmonary inflammatory disease which is common in the elderly. Aging-related alterations have also been found in the structural cells and immune cells of asthma patients although the pathological mechanism of the differential aging-related gene in the development of asthma is still obscure. Of note, DNA methylation (DNAm) have been proven to play an important role in the regulation of aging-related genes. However, the methylation levels of aging-related genes in asthma patients are largely unclear.Methods: First, the mRNA levels and DNAm level of the previous screened 9 aging-related genes in peripheral blood of 51 healthy controls (HCs) and 55 asthmatic patients were detected by multiple targeted bisulfite enrichment sequencing (MethTarget) and qPCR. Secondly, the correlation between the DNAm level of specific altered CpG sites and the pulmonary function indicators of asthma patients was evaluated. Lastly, the Receiver Operator Characteristic (ROC) curve and Principal Component Analysis (PCA) were used to identify the feasibility of the candidate CpG sites as asthma markers.Results: The mRNA expression of the 9 aging-related gene in peripheral blood of asthma patients was significantly different from those of HCs. Besides, the methylation level of the 9 aging-related genes also altered in asthma patients, and a total of 68 CpG sites were related to the severity of asthma. Notably, 10 of the 68 CpG sites had a significant relationship with pulmonary function parameters. Moreover, ROC curve and PCA analysis showed that the candidate differential methylation sites (DMSs) can be used as potential biomarkers for asthma.Conclusions:In summary, this study confirmed the changes in the mRNA expression and DNAm level of aging-related genes in asthma patients. The differential DMSs are associated with the clinical evaluation indicators of asthma, which may indicate the involvement of aging-related genes in the pathogenesis of asthma and provide some new possible biomarker of asthma.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 78%

Variable Expressed Methylation Sites of Aging-related Genes in Asthma

Yang¹,

Lin²,

Yang³

et al. 2020

Preprint

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“…Thereby, gastrodin has been considered as a potential therapeutic agent for diverse diseases such as Tourette syndrome, 7 myocardial infarction, 8 alcoholic liver disease 6,9 and acute lung injury. [11][12][13] For instance, in vivo and in vitro data demonstrated that miR-3202 could protect smokers from COPD. microRNAs (miRNAs) are a sort of small non-coding RNAs that are latterly discovered.…”

mentioning

confidence: 99%

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Qiao

Wang

et al. 2019

J Cellular Molecular Medi

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The beneficial function of gastrodin towards many inflammatory diseases has been identified. This study designed to see the influence of gastrodin in a cell model of chronic obstructive pulmonary disease (COPD). MRC‐5 cells were treated by LPS, before which gastrodin was administrated. The effects of gastrodin were evaluated by conducting CCK‐8, FITC‐PI double staining, Western blot, qRT‐PCR and ELISA. Besides this, the downstream effector and signalling were studied to decode how gastrodin exerted its function. And dual‐luciferase assay was used to detect the targeting link between miR‐103 and lipoprotein receptor‐related protein 1 (LRP1). LPS induced apoptosis and the release of MCP‐1, IL‐6 and TNF‐α in MRC‐5 cells. Pre‐treating MRC‐5 cells with gastrodin attenuated LPS‐induced cell damage. Meanwhile, p38/JNK and NF‐κB pathways induced by LPS were repressed by gastrodin. miR‐103 expression was elevated by gastrodin. Further, the protective functions of gastrodin were attenuated by miR‐103 silencing. And LRP1 was a target of miR‐103 and negatively regulated by miR‐103. The in vitro data illustrated the protective function of gastrodin in LPS‐injured MRC‐5 cells. Gastrodin exerted its function possibly by up‐regulating miR‐103 and modulating p38/JNK and NF‐κB pathways.

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“…MiR-203a-3p served as a target of LINC00342 to inhibit cell proliferation, colony formation, migration and invasion in non-small cell lung cancer [32]. Recently, bioinformatics analysis indicated that the expression of miR-203a-3p was dramatically decreased in the bronchial epithelial cells [14]. Therefore, it is imperative to disclose the role of miR-203a-3p in asthma.…”

Section: Discussionmentioning

confidence: 99%

“…Also, Chen et al demonstrated that miR-203a-3p was a novel molecular therapeutic target of colorectal cancer, which has been proved to enhance colorectal cancer proliferation and migration [13]. Besides that, bio-informatics analysis revealed that the expression of miR-203a-3p was decreased evidently in the bronchial epithelial cells, indicating that miR-203a-3p might be the potential target for the treatment of asthma [14]. However, the function and molecular mechanism of miR-203a-3p in the development of asthma need further study.…”

Section: Introductionmentioning

confidence: 99%

MiR-203a-3p regulates TGF-β1-induced epithelial–mesenchymal transition (EMT) in asthma by regulating Smad3 pathway through SIX1

Fan

2020

Bioscience Reports

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Asthma is a common chronic airway disease with increasing prevalence. MicroRNAs act as vital regulators in cell progressions and have been identified to play crucial roles in asthma. The objective of the present study is to clarify the molecular mechanism of miR-203a-3p in the development of asthma. The expression of miR-203a-3p and Sine oculis homeobox homolog 1 (SIX1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of SIX1, fibronectin, E-cadherin, vimentin, phosphorylated-drosophila mothers against decapentaplegic 3 (p-Smad3) and Smad3 were measured by Western blot. The interaction between miR-203a-3p and SIX1 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. MiR-203a-3p was down-regulated and SIX1 was up-regulated in asthma serums, respectively. Transforming growth factor-β1 (TGF-β1) treatment induced the reduction of miR-203a-3p and the enhancement of SIX1 in BEAS-2B and 16HBE cells in a time-dependent manner. Subsequently, functional experiments showed the promotion of epithelial–mesenchymal transition (EMT) induced by TGF-β1 treatment could be reversed by miR-203a-3p re-expression or SIX1 deletion in BEAS-2B and 16HBE cells. SIX1 was identified as a target of miR-203a-3p and negatively regulated by miR-203a-3p. Then rescue assay indicated that overexpressed miR-203a-3p ameliorated TGF-β1 induced EMT by regulating SIX1 in BEAS-2B and 16HBE cells. Moreover, miR-203a-3p/SIX1 axis regulated TGF-β1 mediated EMT process in bronchial epithelial cells through phosphorylating Smad3. These results demonstrated that MiR-203a-3p modulated TGF-β1-induced EMT in asthma by regulating Smad3 pathway through targeting SIX1.

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Deducting MicroRNA-Mediated Changes Common in Bronchial Epithelial Cells of Asthma and Chronic Obstructive Pulmonary Disease—A Next-Generation Sequencing-Guided Bioinformatic Approach

Cited by 38 publications

References 67 publications

Variable Expressed Methylation Sites of Aging-related Genes in Asthma

Variable Expressed Methylation Sites of Aging-related Genes in Asthma

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

MiR-203a-3p regulates TGF-β1-induced epithelial–mesenchymal transition (EMT) in asthma by regulating Smad3 pathway through SIX1

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