ArticleJournal of cellular and molecular medicine2021
Transgenic overexpression of ITGB6 in intestinal epithelial cells exacerbates dextran sulfate sodium-induced colitis in mice.
Article in Journal of cellular and molecular medicine, 2021. 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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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Predictors of time to surgical recurrence after ileal or ileocolonic resection in Crohn's disease: role of integrin αvβ6 and development of a predictive nomogram.Updates in surgery · 2026Article
- Characteristics of cell adhesion molecules expression and environmental adaptation in yak lung tissue.Scientific reports · 2025Article
- Characterization and proteomic analysis of plasma-derived small extracellular vesicles in locally advanced rectal cancer patients.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Knockout of integrin αvβ6 protects against renal inflammation in chronic kidney disease by reduction of pro-inflammatory macrophages.Cell death & disease · 2024Article
- Exploring the role of ITGB6: fibrosis, cancer, and other diseases.Apoptosis : an international journal on programmed cell death · 2024Review
- Targeting integrin pathways: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2023Review
- Integrin β6 deficiency protects mice from experimental colitis and colitis-associated carcinoma by altering macrophage polarization.Frontiers in oncology · 2023Article
- Transgenic overexpression of ITGB6 in intestinal epithelial cells exacerbates dextran sulfate sodium-induced colitis in mice.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
Integrins, as a large family of cell adhesion molecules, play a crucial role in maintaining intestinal homeostasis. In inflammatory bowel disease (IBD), homeostasis is disrupted. Integrin αvβ6, which is mainly regulated by the integrin β6 subunit gene (ITGB6), is a cell adhesion molecule that mediates cell-cell and cell-matrix interactions. However, the role of ITGB6 in the pathogenesis of IBD remains elusive. In this study, we found that ITGB6 was markedly upregulated in inflamed intestinal tissues from patients with IBD. Then, we generated an intestinal epithelial cell-specific ITGB6 transgenic mouse model. Conditional ITGB6 transgene expression exacerbated experimental colitis in mouse models of acute and chronic dextran sulphate sodium (DSS)-induced colitis. Survival analyses revealed that ITGB6 transgene expression correlated with poor prognosis in DSS-induced colitis. Furthermore, our data indicated that ITGB6 transgene expression increased macrophages infiltration, pro-inflammatory cytokines secretion, integrin ligands expression and Stat1 signalling pathway activation. Collectively, our findings revealed a previously unknown role of ITGB6 in IBD and highlighted the possibility of ITGB6 as a diagnostic marker and therapeutic target for IBD.
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Registered trials
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