ArticleMolecular medicine reports2019
MicroRNA‑146a as a potential regulator involved in the pathogenesis of atopic dermatitis.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- MicroRNAs in atopic dermatitis: A systematic review.Journal of cellular and molecular medicine · 2020Pooled it
- MicroRNAs in immune-related diseases: mechanism, functions and therapeutic perspectives.Frontiers in immunology · 2026Review
- miRNA-146-a, miRNA-21, miRNA-143, miRNA-29-b and miRNA-223 as Potential Biomarkers for Atopic Dermatitis.Clinics and practice · 2025Article
- The Role of MicroRNA in the Pathogenesis of Atopic Dermatitis.International journal of molecular sciences · 2025Review
- Decoding Macrophage Dynamics: A Pathway to Understanding and Treating Inflammatory Skin Diseases.International journal of molecular sciences · 2025Review
- The role of microRNAs in atopic dermatitis.Non-coding RNA research · 2024Review
- Deregulation of MicroRNA-146a and 155 expression levels might underlie complicated pregnancy in Toxoplasma Gondii seronegative women.BMC women's health · 2024Article
- The Interaction between the Host Genome, Epigenome, and the Gut-Skin Axis Microbiome in Atopic Dermatitis.International journal of molecular sciences · 2023Review
- Genomic, Epigenomic, Transcriptomic, Proteomic and Metabolomic Approaches in Atopic Dermatitis.Current issues in molecular biology · 2023Review
- Intrinsic Effects of Exposome in Atopic Dermatitis: Genomics, Epigenomics and Regulatory Layers.Journal of clinical medicine · 2023Review
- The Essential Role of microRNAs in Inflammatory and Autoimmune Skin Diseases-A Review.International journal of molecular sciences · 2023Review
- Blood-Based Biomarkers for Eosinophilic Esophagitis and Concomitant Atopic Diseases: A Look into the Potential of Extracellular Vesicles.International journal of molecular sciences · 2023Review
- miR-146a, miR-221, and miR-155 are Involved in Inflammatory Immune Response in Severe COVID-19 Patients.Diagnostics (Basel, Switzerland) · 2022Article
- Anti-Inflammatory microRNAs for Treating Inflammatory Skin Diseases.Biomolecules · 2022Review
- Post-Translational Modifications in Atopic Dermatitis: Current Research and Clinical Relevance.Frontiers in cell and developmental biology · 2022Review
- Genetic and Epigenetic Aspects of Atopic Dermatitis.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have demonstrated that microRNA (miR)‑146a is involved in the inflammatory response of atopic dermatitis (AD). The aim of the present study was to investigate the expression of miR‑146a in the serum of patients with AD and in skin lesions of AD animal models. In addition, we aimed to predict and verify the target genes of miR‑146a. miR‑146a expression was measured in AD patient serum via reverse transcription‑quantitative PCR. T‑helper (Th)1 [CD4+; interferon (IFN)‑γ+] and Th2 [CD4+; interleukin (IL)‑4+] expression in peripheral blood mononuclear cells was evaluated using flow cytometry. Following the establishment of a 2,4‑dinitrofluorobenzene‑induced C57BL/6 mouse AD model, Th1 (CD4+IFN‑γ+) and Th2 (CD4+IL‑4+) expression was analyzed in murine spleen cells via flow cytometry. Plasmids were transfected into 293T cells and at 48 h post‑transfection, cells were analyzed using a luciferase assay system. The results revealed that the AD group had a significantly lower Th1/Th2 ratio and a significantly higher miR‑146a expression compared with the control group (P<0.05). Furthermore, a decreased Th1/Th2 ratio and a significantly increased miR‑146a expression were observed in the model group compared with the control group (P<0.01). We also conducted a dual‑luciferase assay to determine whether small ubiquitin‑related modifier 1 (SUMO1) if the target gene of miR‑146a. We observed a ~30% decrease in the relative luciferase activity in cells containing the 3'‑untranslated region of SUMO1 + miR‑146a). The results of the luciferase assay indicated that may be a direct mRNA target of miR‑146a; however, the quantification of band density of SUMO1 expression following western blotting did not significantly differ. The development of animal models in AD research is of vital importance. The results revealed that miR‑146a may be a potential regulator involved in the pathogenesis of AD. Furthermore, the current study determined that miR‑146a could be a valuable marker of AD and thus, may be applied in the development of therapeutic strategies for treating AD.
Indexed as
Identifiers
What OpenQuestion holds
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.