ArticleExperimental & molecular medicine2015
MiR-155 modulates the inflammatory phenotype of intestinal myofibroblasts by targeting SOCS1 in ulcerative colitis.
Article in Experimental & molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 120 citations in OpenAlex.
- Dicer-independent miR-451a is upregulated in periodontitis and potentiates inflammation by impairing macrophage polarization and SOCS activity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Scaffold-mediated miRNA-155 inhibition promotes regenerative macrophage polarisation leading to anti-inflammatory, angiogenic and neurogenic responses for wound healing.Bioactive materials · 2026Article
- Mapping the Ischemic Continuum: Dynamic Multi-Omic Biomarker and AI for Personalized Stroke Care.International journal of molecular sciences · 2026Review
- MicroRNAs in immune-related diseases: mechanism, functions and therapeutic perspectives.Frontiers in immunology · 2026Review
- Interplay Between Dysregulated Immune System and the Footprints of Blood-Borne miRNAs in Treatment Naive Crohn's Disease and Ulcerative Colitis Patients.International journal of molecular sciences · 2025Article
- MicroRNA-122 overexpression suppresses the colon cancer cell proliferation by downregulating the astrocyte elevated gene-1/metadherin oncoprotein.Annals of medicine · 2025Article
- Review
- Milk-Derived Extracellular Vesicles and microRNAs: Potential Modulators of Intestinal Homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Toward Precision Medicine: Molecular Biomarkers of Response to Tofacitinib in Inflammatory Bowel Disease.Genes · 2025Review
- Probiotics Exert Gut Immunomodulatory Effects by Regulating the Expression of Host miRNAs.Probiotics and antimicrobial proteins · 2025Review
- MicroRNA-microbiota interactions: Emerging strategies for modulating intestinal homeostasis and enhancing host health.iMetaOmics · 2025Review
- Chronic Gastrointestinal Disorders and miRNA-Associated Disease: An Up-to-Date.International journal of molecular sciences · 2025Review
- Identification and validation of biomarkers related to centrosome replication in ulcerative colitis based on bulk transcriptome, single-cell RNA sequencing and experiments.Frontiers in immunology · 2025Article
- Article
- MicroRNA signatures in the pathogenesis and therapy of inflammatory bowel disease.Clinical and experimental medicine · 2024Review
- Expression Changes of miRNAs in Humans and Animal Models of Amyotrophic Lateral Sclerosis and Their Potential Application for Clinical Diagnosis.Life (Basel, Switzerland) · 2024Review
- miR-155 and miR-21 as Diagnostic and Therapeutic Biomarkers for Ulcerative Colitis: There Is Still a Long Way to Go.Biomedicines · 2024Article
- MicroRNAs in inflammatory bowel disease: What do we know and what can we expect?World journal of gastroenterology · 2024Article
- Exploring the role of IL-1β in inflammatory bowel disease pathogenesis.Frontiers in medicine · 2024Review
- A mutual regulatory loop between miR-155 and SOCS1 influences renal inflammation and diabetic kidney disease.Molecular therapy. Nucleic acids · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal levels of microRNA (miR)-155, which regulate inflammation and immune responses, have been demonstrated in the colonic mucosa of patients with inflammatory bowel diseases (IBD), although its role in disease pathophysiology is unknown. We investigated the role of miR-155 in the acquisition and maintenance of an activated phenotype by intestinal myofibroblasts (IMF), a key cell population contributing to mucosal damage in IBD. IMF were isolated from colonic biopsies of healthy controls, ulcerative colitis (UC) and Crohn's disease (CD) patients. MiR-155 in IMF was quantified by quantitative reverse transcription-PCR in basal condition and following exposure to TNF-α, interleukin (IL)-1β, lipopolysaccharide (LPS) or TGF-β1. The effects of miR-155 mimic or inhibitor transfection on cytokine release and suppressor of cytokine signaling 1 (SOCS1) expression were assessed by enzyme-linked immunosorbent assay and western blot, respectively. Regulation of the target gene SOCS1 expression by miR-155 was assessed using luciferase reporter construct. We found that miR-155 was significantly upregulated in UC as compared with control- and CD-derived IMF. Moreover, TNF-α and LPS, but not TGF-β1 and IL-1β, significantly increased miR-155 expression in IMF. Ectopic expression of miR-155 in control IMF augmented cytokines release, whereas it downregulated SOCS1 expression. MiR-155 knockdown in UC-IMF reduced cytokine production and enhanced SOCS1 expression. Luciferase reporter assay demonstrated that miR-155 directly targets SOCS1. Moreover, silencing of SOCS1 in control IMF significantly increased IL-6 and IL-8 release. In all, our data suggest that inflammatory mediators induce miR-155 expression in IMF of patients with UC. By downregulating the expression of SOCS1, miR-155 wires IMF inflammatory phenotype.
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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.