ArticleMolecular biology reports2022
MiR-155-5p modulates inflammatory phenotype of activated oral lichen-planus-associated-fibroblasts by targeting SOCS1.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 10 citations in OpenAlex.
- Shenfu Injection Inhibits Cardiac Fibroblast Activation and Improves Myocardial Fibrosis by Down-regulating M1 Macrophage-Derived Exosomal miR-155-5p.Cardiovascular drugs and therapy · 2026Article
- [Effect of miR-155-5p regulating the TLR4/MAPK/NF-κB pathway on inflammatory response, coronary artery lesion and immune function in mice with Kawasaki disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
- The miR-155-5p/SOCS1/NF-κB Axis Regulates Airway Smooth Muscle Dysfunction and is a Potential Therapeutic Candidate of Chronic Obstructive Pulmonary Disease.Inflammation · 2026Article
- miR-155 targets SOCS1 to modulate the phenotype transition of M1 macrophage in distraction osteogenesis promoted by PTH administration.European journal of medical research · 2025Article
- Elucidating the preventive and therapeutic effects of cardiac telocytes paracrine microRNAs on ischemic heart disease.Frontiers in cardiovascular medicine · 2025Article
- Fraxin alleviates oral lichen planus by suppressing OCT3-mediated activation of FGF2/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Upregulation of psoriasin/S100A7 correlates with clinical severity in patients with oral lichen planus.Clinical oral investigations · 2024Article
- Non-Coding RNAs as Potential Targets for Diagnosis and Treatment of Oral Lichen Planus: A Narrative Review.Biomolecules · 2023Review
- Network analysis identifies circulating miR-155 as predictive biomarker of type 2 diabetes mellitus development in obese patients: a pilot study.Scientific reports · 2023Article
- Immune Cells Release MicroRNA-155 Enriched Extracellular Vesicles That Promote HIV-1 Infection.Cells · 2023Article
- Active Fraction of Polyrhachis Vicina Roger (AFPR) Ameliorate Depression Induced Inflammation Response by FTO/miR-221-3p/SOCS1 Axis.Journal of inflammation research · 2023Article
- Role and mechanism of fibroblast-activated protein-α expression on the surface of fibroblast-like synoviocytes in rheumatoid arthritis.Frontiers in immunology · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOral lichen planus (OLP) is a chronic inflammatory oral mucosal disease. Cytokines are closely associated with OLP development. In addition to immune cells, fibroblasts have been reported to induce regional inflammation. MicroRNA(miR)-155-5p is reportedly increased significantly in OLP and is known to regulate inflammation. This study aimed to investigate the role of miR-155-5p in fibroblasts of OLP lesions. METHODS AND
resultsNormal mucosal fibroblasts (NFs) and OLP associated-fibroblasts (OLP AFs) were isolated from the oral mucosa of 15 healthy controls and 30 OLP patients. We detected the expression of miR-155-5p and fibroblast activation protein alpha (FAP-α) using quantitative RT-PCR and analyzed their correlation. Interleukin (IL)-6 and IL-8 levels were determined using ELISA. Expression of suppressor of cytokine signaling (SOCS) 1 was analyzed by western blotting. A dual-luciferase reporter assay was performed to investigate the interaction between miR-155-5p and SOCS1. MiR-155-5p and FAP-α were significantly increased and positively correlated in OLP AFs. Overexpression of miR-155-5p in OLP AFs augmented IL-6 and IL-8 release and decreased SOCS1 expression, whereas knockdown of miR-155-5p in OLP AFs decreased IL-6 and IL-8 release. The expression of SOCS1 was downregulated in OLP AFs, and SOCS1 silencing augmented IL-6 and IL-8 production in OLP AFs. Furthermore, miR-155-5p inhibited SOCS1 expression by directly targeting its 3'-UTR in OLP AFs.
conclusionsMiR-155-5p regulates the secretion of IL-6 and IL-8 by downregulating the expression of SOCS1 in activated OLP AFs. Our results provide novel insights into the pathogenesis of OLP and identify a potential new target for OLP therapy.
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