ArticleExperimental and therapeutic medicine2018
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.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Genetically Predicted Serum miRNAs as Potential Causal Drivers of Atopic Dermatitis: Evidence from Large-Scale GWAS and Clinical Validation.Clinical, cosmetic and investigational dermatology · 2026Article
- Research progress on regulatory mechanisms of mucosal barriers and their applications in allergic diseases.Frontiers in immunology · 2026Review
- Multi-omics in Allergic Rhinitis: Mechanism Dissection and Precision Medicine.Clinical reviews in allergy & immunology · 2025Review
- Fructus Arctii Mitigates Depressive Disorder via the Let-7e-Modulated Toll-Like Receptor (TLR) Signaling Pathway.Brain and behavior · 2024Article
- Article
- The Role of Noncoding RNA in Airway Allergic Diseases through Regulation of T Cell Subsets.Mediators of inflammation · 2022Review
- The Role of Small Extracellular Vesicles and MicroRNAs in the Diagnosis and Treatment of Allergic Rhinitis and Nasal Polyps.Mediators of inflammation · 2022Review
- Genetics and Epigenetics in Allergic Rhinitis.Genes · 2021Review
- Spotlight on microRNAs in allergy and asthma.Allergy · 2021Review
- MicroRNA-29 mediates anti-inflammatory effects and alleviation of allergic responses and symptoms in mice with allergic rhinitis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021Article
- Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway.Bioscience reports · 2021Article
- Polymorphisms in MicroRNA Target Sites of TGF-β Signaling Pathway Genes and Susceptibility to Allergic Rhinitis.International archives of allergy and immunology · 2021Article
- Identification of differentially expressed miRNAs after Lactobacillus reuteri treatment in the ileum mucosa of piglets.Genes & genomics · 2020Article
- Analysis the effect of miR-141-3p/HMGB1 in LPS-induced mucus production and the apoptosis in nasal epithelial cells.The Kaohsiung journal of medical sciences · 2020Article
- MicroRNAs: Potential Biomarkers and Targets of Therapy in Allergic Diseases?Archivum immunologiae et therapiae experimentalis · 2019Review
- Review
- Observational
- Toll-Like Receptor and miRNA-let-7e Expression Alter the Inflammatory Response inFrontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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