Dataset Information

Long non-coding RNA growth arrest-specific 5 and its targets, microRNA-21 and microRNA-140, are potential biomarkers of allergic rhinitis.

ABSTRACT:

Objective

Long non-coding RNA growth arrest-specific 5 (lnc-GAS5) and its targets (microRNA [miR]-21 and miR-140) are involved in the development and progression of allergic rhinitis (AR). However, the correlation of lnc-GAS5 with miR-21 and miR-140 and their associations with disease risk, symptom severity, and Th1/Th2 cytokines in AR remain unclear. Thus, this study aimed to investigate this topic.

Methods

In total, 120 patients with AR and 60 controls were recruited. Nasal-mucosa tissues were collected from all participants. Lnc-GAS5, its targets (miR-21 and miR-140), interferon (IFN)-γ, interleukin (IL)-2, IL-4, and IL-10 were detected by reverse-transcription quantitative polymerase chain reaction.

Results

Lnc-GAS5 was elevated, while miR-21 and miR-140 was downregulated in AR patients than in controls (p < 0.001). In AR patients, lnc-GAS5 was negatively correlated with miR-21 (p < 0.001), miR-140 (p < 0.001), IFN-γ (p = 0.019), and IL-2 (p = 0.039) and positively correlated with IL-4 (p = 0.004) and IL-10 (p < 0.001), individual nasal symptom scores (INSSs) for itching, sneezing, and congestion (p < 0.05), and total nasal symptom score (TNSS) (p < 0.001). Moreover, miR-21 and miR-140 were negatively correlated with some INSSs, total TNSS score, and IL-10 and positively correlated with IFN-γ and IL-2 (p < 0.05).

Conclusion

Lnc-GAS5 is negatively correlated with that of its targets (miR-21 and miR-140) in AR; meanwhile, lnc-GAS5, miR-21, and miR-140 are correlated with disease risk, symptom severity, and Th1/Th2 imbalance in AR, suggesting the potential of these biomarkers in the development and progression of AR.

SUBMITTER: Song J

PROVIDER: S-EPMC8529140 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature

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Publications

Long non-coding RNA growth arrest-specific 5 and its targets, microRNA-21 and microRNA-140, are potential biomarkers of allergic rhinitis.

Song Ji J Wang Taojiao T Chen Yandan Y Cen Ruixiang R

Journal of clinical laboratory analysis 20210902 10

<h4>Objective</h4>Long non-coding RNA growth arrest-specific 5 (lnc-GAS5) and its targets (microRNA [miR]-21 and miR-140) are involved in the development and progression of allergic rhinitis (AR). However, the correlation of lnc-GAS5 with miR-21 and miR-140 and their associations with disease risk, symptom severity, and Th1/Th2 cytokines in AR remain unclear. Thus, this study aimed to investigate this topic.<h4>Methods</h4>In total, 120 patients with AR and 60 controls were recruited. Nasal-muco ...[more]

PMID: 34473845

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Project description:BackgroundAllergic rhinitis (AR) is an upper respiratory tract inflammation disease caused by IgE-mediated reactions against inhaled allergens. The incidence of AR is significantly increasing throughout the world. Hence, more specific, and sensitive gene biomarkers and understanding the underlying pathways are necessary to further explore the AR pathogenesis.ObjectiveTo identify gene biomarkers in nasal mucosa and in blood from AR patients which could be used in AR diagnosis.MethodsThe gene expression profiles of GSE43523 from nasal epithelial cells and GSE75011 from Th2-enriched CD4+ T cells in blood were downloaded from the Gene Expression Omnibus database. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses and protein-protein interaction (PPI) network analysis were conducted to investigate the functional changes of genes. The receiver operating characteristic (ROC) curves were used to assess the diagnostic values of the hub genes. Real-time quantitative PCR (RT-qPCR) was performed to validate the hub genes.ResultsSignificant differentially enriched gene signatures in AR patients were identified in nasal epithelial cells (n-DEGs) and in blood (t-DEGs). Signatures associated with axoneme, extracellular matrix, collagen fibril organization, cell motility, calcium ion binding, and so on were more enriched in n-DEGs, whereas signatures associated with TNF signaling pathway, detoxification of inorganic compound, and cellular response to corticotropin-releasing hormone stimulus were enriched in t-DEGs. In addition, we identified 8 hub genes and 14 hub genes from n-DEGs and t-DEGs, respectively. The combination of POSTN in nasal mucosa and PENK and CDC25A in blood was constructed with a good AR predicting performance. The area under the curve (AUC) of the ROC curve of 3 hub genes' combination was 0.98 for AR diagnosis.ConclusionThis study utilized gene expression profiles and RT-qPCR validation on nasal mucosa and blood from AR patients to investigate the potential biomarkers for AR diagnosis.

Project description:BackgroundAllergic rhinitis (AR) is a pervasive global health issue, and currently, there is a scarcity of targeted drug therapies available. This study aims to identify potential druggable target genes for AR using Mendelian randomization (MR) analysis.MethodsMR analysis was conducted to assess the causal effect of expression quantitative trait loci (eQTL) in the blood on AR. Data on AR were collected from 2 datasets: FinnGen(R9) (11,009 cases and 359,149 controls) and UK Biobank (25,486 cases and 87,097 controls). Colocalization analysis was utilized to assess the common causal genetic variations between the identified drug target genes and AR. We also employed available genome-wide association studies (GWAS) data to gauge the impact of druggable genes on AR biomarkers and other allergic diseases.ResultsThis study employs MR to analyze the relationship between 3410 druggable genes and AR. After Bonferroni correction, 10 genes were found to be significantly associated with AR risk (P < 0.05/3410). Colocalization analysis revealed a significant causal relationship between the expression variation of CFL1 and EFEMP2 genes and AR, sharing direct causal variants (colocalization probability PP.H3 + PP.H4 > 0.8), highlighting their importance as potential therapeutic targets for AR. The CFL1 gene showed a causal link with levels of thymic stromal lymphopoietin (TSLP), eosinophil count, and interleukin-13 (IL-13) (P = 0.016, 7.45E-16, 0.00091, respectively). EFEMP2 was also causally related to eosinophil count, IL-13, and interleukin-17 (IL-17) (P = 0.00012, 0.00091, 0.032, respectively). PheWAS analysis revealed significant associations of CFL1 with asthma, whereas EFEMP2 showed associations with both asthma and eczema. Protein-Protein Interaction (PPI) network analysis further unveiled the direct interactions of EFEMP2 and CFL1 with proteins related to immune regulation and inflammatory responses, with 77.64% of the network consisting of direct bindings, indicating their key roles in modulating AR-related immune and inflammatory responses. Notably, there was an 8.01% significant correlation between immune-related pathways and genes involved in inflammatory responses.ConclusionThese genes present notable associations with AR biomarkers and other autoimmune diseases, offering valuable targets for developing new AR therapies.

Dataset Information

Long non-coding RNA growth arrest-specific 5 and its targets, microRNA-21 and microRNA-140, are potential biomarkers of allergic rhinitis.

Objective

Methods

Results

Conclusion

Publications

Long non-coding RNA growth arrest-specific 5 and its targets, microRNA-21 and microRNA-140, are potential biomarkers of allergic rhinitis.

Similar Datasets

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