ArticleInflammatory bowel diseases2011
STAT6 activation in ulcerative colitis: a new target for prevention of IL-13-induced colon epithelial cell dysfunction.
Article in Inflammatory bowel diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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70 citing papers in PubMed, 108 citations in OpenAlex.
- Intestinal epithelial cell-specific deletion of Jak2 disrupts gut homeostasis.Scientific reports · 2026Article
- Immune-microbe interactions in pediatric ulcerative colitis: clinical features, pathogenesis, and novel targeted therapeutic strategies.Frontiers in immunology · 2026Review
- The Multifaceted Roles of STAT6: Implications for Precision Immunotherapeutics.ImmunoTargets and therapy · 2026Review
- Activation of STAT6 in Intestinal Epithelial Cells Predisposes to Gut Inflammation.European journal of immunology · 2025Article
- GPI-anchored serine proteases: essential roles in development, homeostasis, and disease.Biological chemistry · 2025Review
- Strategies for targeting cytokines in inflammatory bowel disease.Nature reviews. Immunology · 2024Review
- Efficacy ofNutrients · 2024Article
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- Sensitization of colonic nociceptors by IL-13 is dependent on JAK and p38 MAPK activity.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Alleviative mechanism and effect ofFood science & nutrition · 2023Article
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- Gut homeostasis, injury, and healing: New therapeutic targets.World journal of gastroenterology · 2022Review
- The effects of the probiotic cocktail on modulation of the NF-kB and JAK/STAT signaling pathways involved in the inflammatory response in bowel disease model.BMC immunology · 2022Article
- A flavonoid rich standardized extract of Glycyrrhiza glabra protects intestinal epithelial barrier function and regulates the tight-junction proteins expression.BMC complementary medicine and therapies · 2022Article
- New Insights Into the Epigenetic Regulation of Inflammatory Bowel Disease.Frontiers in pharmacology · 2022Review
- Glucocorticoid induced group 2 innate lymphoid cell overactivation exacerbates experimental colitis.Frontiers in immunology · 2022Article
- A Novel Role of IL13Rα2 in the Pathogenesis of Proliferative Vitreoretinopathy.Frontiers in medicine · 2022Article
- Phytochemicals Targeting JAK-STAT Pathways in Inflammatory Bowel Disease: Insights from Animal Models.Molecules (Basel, Switzerland) · 2021Review
- Article
10 more citing papers are in PubMed but not listed here.
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9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundInterleukin 13 (IL-13) is upregulated in ulcerative colitis (UC) and increases colon epithelial permeability by inducing apoptosis and expression of the pore-forming tight junction protein claudin-2. IL-13 induces activation of signal transducer and activator of transcription 6 (STAT6). However, the STAT6 phosphorylation status in patients with UC is unknown, as is the effect of STAT6 inhibition on colonic epithelium exposed to IL-13. The study aims were to determine if mucosal STAT6 phosphorylation is increased in patients with UC, and if STAT6 inhibition attenuates IL-13-induced colon epithelial cell dysfunction.
methodsImmunohistochemical staining for phosphorylated (p) STAT6 was performed on colonic tissue from newly diagnosed pediatric subjects with UC (early UC) or Crohn's disease (CD), colectomy tissue from adults with UC (advanced UC), and controls. Colon HT-29 and T84 cells were transfected with STAT6 small interfering RNA (siRNA), or treated with suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor that inhibits STAT6, prior to IL-13 treatment.
resultsThe median score for epithelial pSTAT6 was 0 in control subjects, 2 in early UC (versus control P = 0.019), 4 in advanced UC (P = 0.003), and 0 in CD (P = 0.4). Cell transfection with STAT6 siRNA prevented IL-13-induced apoptosis and claudin-2 expression. SAHA inhibited IL-13-induced STAT6 phosphorylation, apoptosis, and claudin-2 expression, and mitigated IL-13-induced reductions in transepithelial resistance.
conclusionsUC is associated with increased colonic epithelial STAT6 phosphorylation, and STAT6 inhibition prevents IL-13-induced apoptosis and barrier disruption. These data identify STAT6 as a novel target for UC treatment and support further study of SAHA as a therapeutic agent.
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