ArticleThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2022
MiR-222-3p Aggravates the Inflammatory Response by Targeting SOCS1 to Activate STAT3 Signaling in Ulcerative Colitis.
Article in The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 12 citations in OpenAlex.
- Unraveling the drug resistance web in IBD: The gut microbiota-immunity-epigenetics axis.Gut microbes · 2026Review
- Preliminary miRNA profiling of plasma from patients infected with distinct SARS-CoV-2 variants.Molecular biology reports · 2026Article
- miR-222-3p targeting MEGF9 exacerbates sepsis-induced myocardial injury.Journal of cardiothoracic surgery · 2026Article
- MicroRNA Profiling as a Novel Predictive Tool for Operational Tolerance in Pediatric Liver Transplantation: A Single-center Study.Transplantation direct · 2026Article
- Regulatory Role of IGF2BP2 in Intestinal Mucosal Barrier Dysfunction in Ulcerative Colitis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Moxibustion Regulates the BRG1/Nrf2/HO-1 Pathway by Inhibiting MicroRNA-222-3p to Prevent Oxidative Stress in Intestinal Epithelial Cells in Ulcerative Colitis and Colitis-Associated Colorectal Cancer.Journal of immunology research · 2024Article
- Role of Increased miR-222-3p Expression in Peripheral Blood and Wound Marginal Tissues of Type 2 Diabetes Mellitus Patients with Diabetic Foot Ulcer.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Suppression of microRNA-222-3p ameliorates ulcerative colitis and colitis-associated colorectal cancer to protect against oxidative stressFrontiers in immunology · 2023Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundUlcerative colitis is characterized by relapsing inflammation in the gastrointestinal tract with limited treatment options. The aim of the present study was to assess the anti-inflammatory effect of Suppressor of cytokine signaling (SOCS1) on lipopolysac- charide-stimulated RAW264.7 cells and to investigate its potential mechanisms.
methodsThe in vitro ulcerative colitis model was established by using lipopolysaccharide-stimulated RAW264.7 cells. Western blot- ting was used to detect the protein expression levels of SOCS1, JAK2, STAT3, and VDR. Reverse transcription-quantitative polymerase chain reaction was used to measure the mRNA expression of SOCS1, miR-222-3p, and VDR. An enzyme-linked immunosorbent assay was performed to measure the levels of inflammatory cytokines. A luciferase assay assessed the binding of SOCS1 to miR-222-3p. A total of 15 patients with ulcerative colitis and 18 healthy controls were recruited. The expression levels of SOCS1 and miR-222-3p in the colonic mucosa tissues of patients with ulcerative colitis and healthy controls were determined by reverse transcription-quantitative polymerase chain reaction.
resultsSOCS1 upregulation inhibited the lipopolysaccharide-induced inflammation in RAW264.7 cells. SOCS1 was confirmed to be tar- geted by miR-222-3p. Silencing SOCS1 significantly abolished the inhibitory effects of miR-222-3p downregulation on inflammation. MiR-222-3p activated STAT3 signaling and reduced VDR expression by targeting SOCS1 in lipopolysaccharide-treated RAW264.7 cells. Additionally, miR-222-3p expression was upregulated in ulcerative colitis patients (P = 5.16E-10), while SOCS1 (P = 2.75E-10) and VDR (P = 52.5E-9) expression was downregulated in ulcerative colitis patients. Endoscopic scores (UCEIS) revealed significant positive cor- relation with miR-222-3p and negative correlation with SOCS1 and VDR.
conclusionMiR-222-3p targets SOCS1 to aggravate the inflammatory response by suppressing VDR and activating STAT3 signaling in ulcerative colitis.
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