Aberrant expressions of circulating lncRNA NEAT1 and microRNA‐125a are linked with Th2 cells and symptom severity in pediatric allergic rhinitis

Wu, Xionghui; Zhao, Sheng; Huang, Weiqing; Huang, Lihua; Huang, Min; Luo, Xinyou; Chang, Shu‐Ting

doi:10.1002/jcla.24235

Cited by 10 publications

(9 citation statements)

References 46 publications

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“…In AR, aberrantly expressed circulating lnc-NEAT1 and miR-125a were associated with Th2 cell percentage and symptoms in pediatric AR. 148 In AD, Liew et al found decreased expression of miR-335 in AD lesions compared with healthy control skin. 149 Nuclear factor kappa-B (NF-κB) (p65) is a critical modulator of inflammatory immune response, and miR-124 is associated with inflammatory response and may constitute a new effector and regulator of NF-κB.…”

Section: Mechanismmentioning

confidence: 99%

Pathogenesis of allergic diseases and implications for therapeutic interventions

Wang

Zhou

Zhang

et al. 2023

Sig Transduct Target Ther

102

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Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. Accompanied by high recurrence rates, the steadily rising incidence rates of these diseases are attracting increasing attention. The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. With the rapid development of immunology, molecular biology, and biotechnology, many new biological drugs have been designed for the treatment of allergic diseases, including anti-immunoglobulin E (IgE), anti-interleukin (IL)-5, and anti-thymic stromal lymphopoietin (TSLP)/IL-4, to control symptoms. For doctors and scientists, it is becoming more and more important to understand the influencing factors, pathogenesis, and treatment progress of allergic diseases. This review aimed to assess the epidemiology, pathogenesis, and therapeutic interventions of allergic diseases, including AR, AAS, AD, and FA. We hope to help doctors and scientists understand allergic diseases systematically.

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Section: Mechanismmentioning

confidence: 99%

Pathogenesis of allergic diseases and implications for therapeutic interventions

Wang

Zhou

Zhang

et al. 2023

Sig Transduct Target Ther

102

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“…Thirdly, a deeper understanding of ncRNAs holds promise for the development of diagnostic tools and treatments for AR is needed. Several other lncRNAs, including lncRNA HCP5, 45 LncRNA MIAT, 46 lncRNA NEAT1, 47 MALAT1, 48 lnc-THRIL, 49 Linc00632, 50 HOTAIRM1, 51 have been implicated in the pathogenesis of AR. Further research is required to confirm whether these lncRNAs interconnect and form a regulatory network that precisely controls the onset and severity of AR.…”

Section: Discussionmentioning

confidence: 99%

LINC00998 Modulating M2 Macrophage Activation in Allergic Rhinitis by Stabilizing BOB.1 mRNA

He,

Tang,

Wen

et al. 2024

JIR

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Background Allergic rhinitis (AR) is globally recognized as a considerable threat to human health with a rising prevalence and a substantial medical and socioeconomic burden. Numerous studies have emphasized the significance of long noncoding RNAs (lncRNAs) in allergic responses. Hence, this research dealt with exploring the involvement of the lncRNA LINC00998 in the mechanism of AR. Methods LINC00998 expression was assessed by qRT-PCR in peripheral blood mononuclear cells acquired from individuals with AR. Additionally, the potential relationship between LINC00998 and macrophage polarization was observed in vitro. Then we constructed AR mice model and macrophage polarization models using THP-1 cells as well as primary human macrophages to verify the M2 shift in AR and the low expression level of LINC00998 in M2 macrophages. We used gain- and loss-of-function experiments to explore the modification of LINC00998 in macrophage polarization. Furthermore, we explored the underlying mechanism of LINC00998 mediates through qRT-PCR, flow cytometry, and Western blot. Results The analysis revealed a significant decrease in LINC00998 expression in the samples obtained from patients with AR. LINC00998 is markedly increased in M1 macrophages whereas decreased in M2 macrophages in vitro. Furthermore, suppression of LINC00998 caused a remarkable enhancement in M2 polarization, whereas its overexpression led to its attenuation. Knockdown of LINC00998 led to a remarkable downregulation of BOB.1 mRNA and protein, while overexpression of LINC00998 upregulated their expression. Moreover, it was found that BOB.1 modulated macrophage polarization through the PU.1/IL-1β axis. Meanwhile, the modulation of LINC00098 overexpression on macrophage polarization and PU.1/ IL-1β can be reversed by BOB.1 siRNA. Conclusion This research revealed the lncRNA LINC00998 altered M2 macrophage polarization by regulating the BOB.1/PU.1/IL-1β axis, which open up new avenues for studying the pathogenesis of AR.

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“…In a recent study, histopathological specimens revealed that lncRNA-NEAT1 expression was significantly upregulated in the nasal mucosa of AR patients and positively correlated with disease symptom scores and inflammatory cytokine levels, suggesting that it could be used as a biomarker to assess the severity of AR disease [140]. Moreover, a recent study found that circulating-derived lncRNAs also 7 Mediators of Inflammation play an essential role in the pathogenesis of AR [147][148][149]. Wang et al [148] found that the exosome-derived lncRNA NEAT1 regulates the microRNA-511/NR4A2 signaling axis and then participates in the disease development of AR.…”

Section: Lncrna and Armentioning

confidence: 99%

The Role of Noncoding RNA in Airway Allergic Diseases through Regulation of T Cell Subsets

Cheng

Tang

Xie

et al. 2022

Mediators of Inflammation

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Allergic rhinitis and asthma are common airway allergic diseases, the incidence of which has increased annually in recent years. The human body is frequently exposed to allergens and environmental irritants that trigger immune and inflammatory responses, resulting in altered gene expression. Mounting evidence suggested that epigenetic alterations were strongly associated with the progression and severity of allergic diseases. Noncoding RNAs (ncRNAs) are a class of transcribed RNA molecules that cannot be translated into polypeptides and consist of three major categories, microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs). Previous studies showed that ncRNAs were involved in the physiopathological mechanisms of airway allergic diseases and contributed to their occurrence and development. This article reviews the current state of understanding of the role of noncoding RNAs in airway allergic diseases, highlights the limitations of recent studies, and outlines the prospects for further research to facilitate the clinical translation of noncoding RNAs as therapeutic targets and biomarkers.

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Aberrant expressions of circulating lncRNA NEAT1 and microRNA‐125a are linked with Th2 cells and symptom severity in pediatric allergic rhinitis

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 10 publications

References 46 publications

Pathogenesis of allergic diseases and implications for therapeutic interventions

Pathogenesis of allergic diseases and implications for therapeutic interventions

LINC00998 Modulating M2 Macrophage Activation in Allergic Rhinitis by Stabilizing BOB.1 mRNA

The Role of Noncoding RNA in Airway Allergic Diseases through Regulation of T Cell Subsets

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