MicroRNA-466a-3p attenuates allergic nasal inflammation in mice by targeting GATA3

Chen, Z; Deng, Yuxiao; Li, F; Xiao, Bokui; Zhou, Xuhong; Tao, Zezhang

doi:10.1111/cei.13312

Cited by 19 publications

(15 citation statements)

References 27 publications

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“…The therapeutic effects of miRNAs on AR have also been reported. miR-466a-3p has been shown to mitigate AR response by inhibiting Th2 cell priming ( 38 ). Furthermore, miR-133b has been demonstrated to alleviate allergic inflammation in AR by targeting NLRP3 ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of miR‑205‑5p alleviates the inflammatory response in allergic rhinitis by targeting B‑cell lymphoma 6

et al. 2021

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allergic rhinitis (ar) is an ige-mediated upper airway disease with a high worldwide prevalence. Microrna (mir)-205-5p upregulation has been observed in ar; however, its role is poorly understood. The aim of the present study was to investigate the effect of mir-205-5p on AR-associated inflammation. To establish an AR model, BalB/c mice were sensitized using an intraperitoneal injection of ovalbumin (oVa) on days 0, 7 and 14, followed by intranasal challenge with oVa on days 21-27. a lentiviral sponge for mir-205-5p was used to downregulate mir-205-5p in vivo via intranasal administration on days 20-26. reverse transcription-quantitative Pcr revealed that mir-205-5p was upregulated in ar mice. notably, mir-205-5p knockdown reduced the frequency of nose-rubbing and sneezing, and attenuated pathological alterations in the nasal mucosa. The levels of total and OVA-specific IgE, cytokines IL-4, IL-5 and IL-13, and inflammatory cells, were decreased by miR-205-5p knockdown in ar mice. in addition, mir-205-5p knockdown inhibited nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation by reducing the expression levels of nlrP3, apoptosis associated speck like protein containing a card, cleaved caspase-1 and il-1β by western blot analysis. B-cell lymphoma 6 (BCL6) was confirmed as a target of miR-205-5p by luciferase reporter assay. In conclusion, the present findings suggested that mir-205-5p knockdown may attenuate the inflammatory response in AR by targeting BCL6, which may be a potential therapeutic target for ar.

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Section: Discussionmentioning

confidence: 99%

Knockdown of miR‑205‑5p alleviates the inflammatory response in allergic rhinitis by targeting B‑cell lymphoma 6

et al. 2021

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“…11 More recently, growing evidence has revealed that the modulation of post-transcriptional regulation by miRNAs is crucial to AR pathogenesis. [12][13][14] Chen et al demonstrated that miR-10b-5p is a novel Th17 regulator and its overexpression inhibits the production of IL-17A in both total CD4 and differentiating Th17 cells. 15 Formaldehyde-induced inflammatory signals originating in the nose were associated with decreased miR-10b levels.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MIAT Promotes Allergic Inflammation and Symptoms by Targeting MiR-10b-5p in Allergic Rhinitis Mice

Lian

Lin

et al. 2021

Am J Rhinol�Allergy

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Background Allergic rhinitis (AR) is one of the most common noninfectious respiratory diseases caused by immunoglobulin E (IgE) response. Objective The study sought to explore the relationship between lncRNA MIAT and miR-10b-5p and their interaction in the regulation of allergic phenotypes in allergic rhinitis (AR) mice. Methods A mice model of AR was constructed using ovalbumin (OVA) sensitization. AR mice were treated with miR-10b-5p agomiR and LNA mediated lncRNA MIAT. The targeting relationship between MIAT and miR-10b-5p was analyzed by the ENCORI website and dual-luciferase reporter assay. The numbers of rubbing and sneezing of mice were counted. Hematoxylin-eosin (HE) staining visualized the eosinophils infiltration in nasal mucosa tissues of mice. The percentage of Th17 cells was quantitated by flow cytometry analysis. ELISA was used to detect the levels of serum OVA-specific IgE, the Th12 cytokine IL-4, and inﬂammatory cytokines (IL-6, IL-17). Results MIAT was up-regulated in the nasal mucosa of AR mice, while miR-10b-5p was down-regulated. MIAT directly suppressed miR-10b-5p expression in AR mice. The numbers of rubbing and sneezing, the percentage of Th17 cells, and the levels of OVA-specific IgE, IL-4, IL-6, and IL-17 in AR mice were decreased by miR-10b-5p overexpression, which was reversed by MIAT overexpression. The eosinophils infiltration in AR mice was inhibited by miR-10b-5p overexpression, which was also reversed by MIAT overexpression. Conclusion The present study demonstrates that MIAT overexpression Promotes allergic inflammation and symptoms by activating Th17 immune response via miR-10b-5p inhibition.

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“…17 A similar study revealed that miR-466a-3p directly suppressed the transcription of GATA-3 and contributed to inadequate Th2 responses in nasal inflammation. 19 miR-466a-3p is a target miRNA of mmu_ circ_0009939, which is a downregulated circRNA identified in this study based on the miRNA binging site prediction. Therefore, it is evident that miRNAs play a critical role in the polarization and activation of T cells.…”

Section: Discussionmentioning

confidence: 88%

“…Some of the predicted miRNAs, such as miR-135a, miR-143, and miR-466a, were conserved miRNAs both in murine and humans and have been previously demonstrated to function in AR development. [17][18][19] Therefore, the circRNAs related to these miRNAs may have an underlying role in AR development.…”

Section: Construction Of a Circrna-mirna Interaction Networkmentioning

confidence: 99%

Altered circular RNA expression profiles in an ovalbumin-induced murine model of allergic rhinitis

Chen

Xiao

et al. 2021

aei

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Background: Emerging evidence shows that circular RNAs (circRNAs) participate in the pathogenesis of multiple immune diseases. However, few studies have focused on the mechanisms of circRNAs involved in allergic rhinitis (AR). Methods: This study performed an RNA sequence (RNA-seq) profiling to identify the expression of circRNAs in nasal mucosa from ovalbumin-induced AR murine models and normal controls. Quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) was then conducted to validate the differential expression of circRNAs. Bioinformatics analysis was applied to demonstrate the biological functions of the dysregulated circRNAs. Results: A total of 86 distinct circRNA candidates were sequenced, of which 51 were upregulated and 35 were downregulated. The T cell receptor, B cell receptor, and calcium signaling pathways may be involved in the pathology of AR. Furthermore, a circRNA-miRNA interaction network was constructed via miRNA response elements analysis. Some circRNAs were cor-related with miRNAs that are involved in T cell polarization and activation, thereby highlighting their potential role in the pathogenesis of AR. Conclusions: This study demonstrates a number of aberrantly expressed circRNAs related to AR, and offers a novel perspective into AR pathogenesis and future therapeutic strategies.

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MicroRNA-466a-3p attenuates allergic nasal inflammation in mice by targeting GATA3

Cited by 19 publications

References 27 publications

Knockdown of miR‑205‑5p alleviates the inflammatory response in allergic rhinitis by targeting B‑cell lymphoma 6

Knockdown of miR‑205‑5p alleviates the inflammatory response in allergic rhinitis by targeting B‑cell lymphoma 6

LncRNA MIAT Promotes Allergic Inflammation and Symptoms by Targeting MiR-10b-5p in Allergic Rhinitis Mice

Altered circular RNA expression profiles in an ovalbumin-induced murine model of allergic rhinitis

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