Microarray Analysis of Differentially Expressed microRNAs in Allergic Rhinitis

Yu, Shiying; Zhang, Ruxin; Liu, Guojun; Zhiqiang, Y.; Hu, Hua; Yu, Shudong; Zhang, Jie

doi:10.2500/ajra.2011.25.3682

Cited by 86 publications

(73 citation statements)

References 25 publications

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“…In this study, miRNAs involved in dermal TDI sensitization were identified using a murine model. A role for miRNAs in airway inflammatory disorders including asthma and allergic rhinitis has recently been described in both human and animal models (Ariel & Upadhyay, 2012;Garbacki et al, 2011;Shaoqing et al, 2011). It has been proposed that the specific mechanism of miRNA action involves a large number of miRNA targeting multiple functionally-related mRNA to orchestrate a co-ordinated regulation of multiple steps in the pathogenesis of asthma, but these processes are not well understood.…”

Section: Discussionmentioning

confidence: 99%

Expression kinetics of miRNA involved in dermal toluene 2,4-diisocyanate sensitization

Anderson

Beezhold

Lukomska

et al. 2013

Journal of Immunotoxicology

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Allergic disease is an important occupational health concern, with work-related asthma and allergic contact dermatitis being the most frequently diagnosed occupational illnesses. Diisocyanates, particularly toluene 2,4-diisocyanate (TDI), have been the leading cause of occupational asthma for many years. Understanding the mechanisms behind allergic disease is critical for treatment and prevention. Recently, the study of post-transcriptional regulation by microRNAs (miRNA) has shed light on mechanisms of allergic disease. The present studies report the expression of miRNA during the sensitization phase of an allergic response to TDI in a murine model. Female BALB/c mice were dermally exposed to TDI (0.1-15% [v/v]) or vehicle. RNA was isolated from superficial parotid lymph nodes at timepoints between 1 h and 15 days post-exposure and then miRNA expression was analyzed using array and real-time quantitative PCR analysis. Consistent changes in miRNA expression were identified for miR-21, miR-22, miR-27b, miR-31, miR-126, miR-155, miR-210, and miR-301a. Following TDI exposure, peak expression was observed by Day 4 for the majority of miRNA evaluated with trends in expression correlated to exposure concentration. Confirmed and predicted targets were identified using Diana-microT, miRanda, miRwalk, and Targetscan algorithms. Evaluation of mRNA expression of cytokine and transcription factor targets suggests that miRNA may have a central role early in TDI sensitization. Understanding the role of these miRNA and their specific mechanism of action in sensitization to TDI may provide pertinent information for the identification of other chemical sensitizers while also contributing to the treatment and prevention of allergic disease.

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Section: Discussionmentioning

confidence: 99%

Expression kinetics of miRNA involved in dermal toluene 2,4-diisocyanate sensitization

Anderson

Beezhold

Lukomska

et al. 2013

Journal of Immunotoxicology

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show abstract

“…The overexpression of miR-142-3p enhances Fc⑀RI-mediated degranulation, and miR-142-3p rescues the reduction of degranulation by silencing Dicer (18). Many miRNA expressions were altered in allergic rhinitis, and differentially expressed miRNAs appear to be involved in the development of allergic rhinitis (19). miR-155 regulates allergic asthma by modulating TH2 response through the transcription factor PU.1 (20).…”

mentioning

confidence: 99%

Transglutaminase II/MicroRNA-218/-181a Loop Regulates Positive Feedback Relationship between Allergic Inflammation and Tumor Metastasis

Eom

Kim

et al. 2014

Journal of Biological Chemistry

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Background:The mechanism of transglutaminase II-mediated allergic inflammation-promoted tumor metastasis remains unknown at the molecular level. Results: The transglutaminase II/miR-218/-181a loop regulates allergic inflammation-promoted tumor metastasis. Conclusion: Transglutaminase II mediates a positive feedback between allergic inflammation and tumor metastasis. Significance: Transglutaminase II can be a target for the development of allergy and cancer therapeutics.

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“…Furthermore, it was observed that miR-let-7e overexpression activated the JAK1/STAT3 signaling pathway. Previous studies have suggested the role of miRNAs in controlling allergic airway inflammation (10,11). The miR-let-7 family of miRNAs is highly conserved across animal species, serving important roles in the regulation of cell proliferation and differentiation (18).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, miRNAs regulate the activity of immune cells within the innate and adaptive immune systems (8,9), and their aberrant expression may result in immune disorders. Previous studies have emphasized the important role of miRNAs in controlling allergic airway inflammation (10,11). Furthermore, Teng et al (12) observed that that miRNA-143 involved in the pathologic process of AR, which was significantly down-regulated in nasal mucosal tissues of AR patients compared with healthy control subjects.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑let‑7e regulates the progression and development of allergic rhinitis by targeting suppressor of cytokine signaling 4 and activating Janus kinase 1/signal transducer and activator of transcription 3 pathway

Zhang

Jiang

et al. 2018

Exp Ther Med

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Abstract. The present study aimed to explore the microRNA-let-7e (miR-let-7e) expression in allergic rhinitis (AR), and to investigate the underlying molecular mechanisms. miR-let-7e expression in the nasal mucosa of mice and patients with AR were detected. The expression levels of three inflammatory factors, including histamine, immunoglobulin E and tumor necrosis factor-α (TNF-α), in the blood of AR mice and in interleukin (IL)-13-stimulated nasal epithelial cells (NECs) were also measured. Furthermore, the target gene of miR-let-7e was predicted and validated using a luciferase reporter assay. The expression levels of Janus kinase 1 (JAK1) and signal transducer and activator of transcription 3 (STAT3) were detected. The results demonstrated that miR-let-7e was downregulated in patients and mice with AR compared with the controls. In addition, the expression levels of inflammatory factors were higher in the blood of mice with AR compared with the control group, while miR-let-7e overexpression inhibited these levels in AR mice and IL-13-stimulated NECs. Furthermore, suppressor of cytokine signaling 4 (SOCS4) was revealed as a potential target gene of miR-let-7e and was negatively regulated by miR-let-7e. Overexpression of SOCS4 abrogated the anti-inflammatory activity of miR-let-7e overexpression. Finally, miR-let-7e overexpression activated the JAK1/STAT3 signaling pathway. In conclusion, miR-let-7e may serve an important role in the progression and development of AR, while overexpression of miR-let-7e had an anti-inflammatory effect by targeting SOCS4, which may be achieved by activation of the JAK1/STAT3 signaling pathway.

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Microarray Analysis of Differentially Expressed microRNAs in Allergic Rhinitis

Cited by 86 publications

References 25 publications

Expression kinetics of miRNA involved in dermal toluene 2,4-diisocyanate sensitization

Expression kinetics of miRNA involved in dermal toluene 2,4-diisocyanate sensitization

Transglutaminase II/MicroRNA-218/-181a Loop Regulates Positive Feedback Relationship between Allergic Inflammation and Tumor Metastasis

MicroRNA‑let‑7e regulates the progression and development of allergic rhinitis by targeting suppressor of cytokine signaling 4 and activating Janus kinase 1/signal transducer and activator of transcription 3 pathway

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