ArticleMolecular medicine (Cambridge, Mass.)2018
OSMR gene effect on the pathogenesis of chronic autoimmune Urticaria via the JAK/STAT3 pathway.
Article in Molecular medicine (Cambridge, Mass.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
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- When ISG15 is involved in inflammation.Frontiers in immunology · 2026Review
- Therapeutic expansion of JAK inhibitors in Chinese dermatological practice: beyond atopic dermatitis to novel autoimmune frontiers.Frontiers in medicine · 2026Review
- Pathophysiologic Mechanisms and Targeted Treatments Associated with the Nervous System in Cutaneous Allergic Diseases.Clinical reviews in allergy & immunology · 2025Review
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- Beyond Antihistamines: How Biologic and Small-Molecule Therapies Are Transforming Chronic Spontaneous Urticaria Care in Adults.Clinical drug investigation · 2025Review
- Is there a role of genetics in acute and chronic urticaria-A systematic review and meta-analysis.Clinical and translational allergy · 2025Article
- Beyond the itch: the complex interplay of immune, neurological, and psychological factors in chronic urticaria.Journal of neuroinflammation · 2025Review
- Transcriptomic and proteomic analysis reveals the mechanism of chicken cecum response toiScience · 2025Article
- Knockdown of miR-155 alleviates skin damage in rats with chronic spontaneous urticaria by modulating the JAK/STAT signaling pathway.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2024Article
- Mining the potential therapeutic targets for COVID-19 infection in patients with severe burn injuries via bioinformatics analysis.International wound journal · 2023Article
- Article
- Neuroimmune interactions in atopic and allergic contact dermatitis.The Journal of allergy and clinical immunology · 2023Review
- Key genes and immune infiltration in chronic spontaneous urticaria: a study of bioinformatics and systems biology.Frontiers in immunology · 2023Article
- Oncostatin M Receptor as a Therapeutic Target for Radioimmune Therapy in Synovial Sarcoma.Pharmaceuticals (Basel, Switzerland) · 2022Article
- STAT3 gain-of-function is not responsible for low total IgE levels in patients with autoimmune chronic spontaneous urticaria.Frontiers in immunology · 2022Article
- lncRNA MSTRG.29039.1 Promotes Proliferation by Sponging hsa-miR-12119 via JAK2/STAT3 Pathway in Multiple Myeloma.Oxidative medicine and cellular longevity · 2021Article
- Review
- Global gene expression profiling of blast lung injury of goats exposed to shock wave.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2020Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic autoimmune urticaria (CAU) is a common skin disease and remains unclear understanding of pathogenesis in the vast majority of cases. In order to explore a new therapy for CAU, the current study was performed to investigate the possible functioning of the Oncostatin M receptor (OSMR) gene in the autoimmunity of CAU via regulation of the JAK/STAT3 signaling pathway.
methodsCAU skin tissues from 24 CAU patients and normal skin tissues from normal subjects were collected. Hematoxylin-eosin (HE) staining was conducted to count eosinophils, and immunohistochemistry was carried out to detect the positive rate of OSMR expression in two kinds of skin tissues. A total of 72 Kunming (KM) mice were selected, and 60 mice were used for establishing CAU models and later transfected with different plasmids. The expression of inflammatory factors was evaluated by enzyme-linked immunosorbent assays (ELISA). Expressions of janus kinase (JAK), signal transducer and activator of transcription 3 (STAT3), interferon-stimulated gene 15 (ISG15), CT10-regulated kinase (CRK), and interferon regulatory factor 9 (IRF9) were identified using Western blot assay and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Epithelial cell proliferation was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, and cell cycle distribution and cell apoptosis were assessed using flow cytometry.
resultsThe findings confirm that OSMR protein expression and histamine release rate are highly elevated in human CAU skin tissues, and the expression of the JAK/STAT3 signaling pathway-related genes (OSMR, JAK2, STAT3, ISG15, CRK and IRF9) was up-regulated. OSMR gene silencing in CAU mice significantly decreases the content of inflammatory factors (IL-1, IL-6, IFN-γ, and IgE), the number of eosinophils, and reduces the expression of the JAK/STAT3 signaling pathway related genes, and further enhances cell proliferation, promotes cell cycle entry and inhibits apoptosis of epithelial cells.
conclusionAll aforementioned results indicate that OSMR gene silencing inhibits the activation of the JAK/STAT3 signaling pathway, thereby suppressing the development of CAU.
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