ArticleAllergy & rhinology (Providence, R.I.)2017
Differential expression of microRNAs and their possible roles in patients with chronic idiopathic urticaria and active hives.
Article in Allergy & rhinology (Providence, R.I.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Differential MicroRNA Expression in Chronic Spontaneous Urticaria in Relation to Treatment Response.Allergy, asthma & immunology research · 2026Article
- Distinct Serum MicroRNA Signatures and mRNA Decay Pathway Dysregulation in NSAID-Exacerbated Chronic Urticaria.International journal of molecular sciences · 2026Article
- Detection of miRNA in chronic spontaneous urticaria patients - pilot study.Frontiers in immunology · 2026Article
- Chromatin accessibility profiling of Treg cells in acute urticaria.Epigenetics · 2025Article
- Dynamic proximity interaction profiling suggests that YPEL2 is involved in cellular stress surveillance.Protein science : a publication of the Protein Society · 2024Article
- Ribosome Biogenesis and Cancer: Insights into NOB1 and PNO1 Mechanisms.Current pharmaceutical design · 2024Review
- In chronic spontaneous urticaria, IgE and C-reactive protein are linked to distinct microRNAs and interleukin-31.Clinical and translational allergy · 2023Article
- Review
- Anti-Inflammatory microRNAs for Treating Inflammatory Skin Diseases.Biomolecules · 2022Review
- Exploring Long Non-Coding RNAs Associated with IP3/DAG Signaling Pathway as Potential Biomarkers Involved in Mast Cell Degranulation in Chronic Spontaneous Urticaria with 2-Year Follow-Up.Journal of inflammation research · 2022Article
- Eosinophil microRNAs Play a Regulatory Role in Allergic Diseases Included in the Atopic March.International journal of molecular sciences · 2020Article
- Biomarkers In Chronic Spontaneous Urticaria: Current Targets And Clinical Implications.Journal of asthma and allergy · 2019Article
- Genome-wide Target Enrichment-aided Chip Design: a 66 K SNP Chip for Cashmere Goat.Scientific reports · 2017Article
- miRNA: The Next Frontier in Dermatology Research and Therapeutics.Indian journal of dermatologyReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic idiopathic urticaria (CIU) is a complicated skin disease with unknown pathophysiology. MicroRNAs (miRNA) have been shown to be active in cellular regulation. The goal of this pilot study was to examine whether miRNAs may be involved in the regulation of CIU or as biomarkers for CIU.
methodsFour groups of three patients each were selected: patients with either active hives or no hives and with positive or negative chronic urticaria (CU) index results. MiRNAs were isolated from patient plasma and analyzed by using miRNA microarray technology to determine the amount of each of the 2567 known human miRNAs.
resultsA total of 16 miRNAs were found to be differentially expressed in patients with active hives. Among them, five (2355-3p, 4264, 2355-5p, 29c-5p, and 361-3p) were significantly increased in samples with positive CU index results, which could be useful biomarkers for patients with chronic autoimmune urticaria. The miRNA data bases were used to find the targets of these selected miRNA sequences. These potential targets were then compared against a list of 154 urticaria-related genes. Twenty-five genes were found to match. These included eight that were significantly downregulated and eight that were significantly upregulated; however, seven of the eight downregulated genes (FBXL20, OPHN1, YPEL2, STARD9, EZH1, KLHL24, ING4) and five of the eight upregulated genes (BYSL, PNO1, ADAMTS9, STEAP4, SRGN) have no reported roles in signaling. For the 13 genes with reported roles in signaling, the following pathways were found: transforming growth factor beta signaling pathway (NRC31, KITLG, THBS1, CCL2), glucocorticoid receptor signaling pathway (NR3C1, SELE, CCL2), p53 signaling pathway (CCNG2, THBS1, CCL2), p21-activated kinase pathway (PAK1IP1, KITLG, CCL2), phosphoinositide-3 kinase protein kinase B signaling pathway (KITLG, CHRM, THBS1), and neuroactive ligand-receptor interaction (NRC31, HRH1, CHRM), which could play important roles in CIU.
conclusionA better understanding of those genes with undefined function and simultaneous quantitation of both miRNAs and messenger RNAs are needed to fully understand CIU disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.