ArticleMediators of inflammation2023
Vitronectin Destroyed Intestinal Epithelial Cell Differentiation through Activation of PDE4-Mediated Ferroptosis in Inflammatory Bowel Disease.
Article in Mediators of inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanostimulatory Cues Determine Intestinal Fibroblast Fate and Profibrotic Remodeling in a Physiodynamic Human Gut-on-a-Chip.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Intestinal Epithelial Cell Ferroptosis in Ulcerative Colitis: Pathogenesis, Signaling Networks, and Therapeutic Implications.Current medical science · 2026Review
- Mechanistic Networks, Cellular Specificity, and Therapeutic Opportunities of Ferroptosis in Ulcerative Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Up-regulated vitronectin in Kawasaki disease shock syndrome serves as a potential biomarker.Translational pediatrics · 2025Article
- Peste des petits ruminants virus (PPRV) induces ferroptosis via LONP1-mediated mitochondrial GPX4 degradation in cell culture.Journal of virology · 2025Article
- The metabolites of gut microbiota: their role in ferroptosis in inflammatory bowel disease.European journal of medical research · 2025Review
- SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.Aging and disease · 2025Review
- Article
- Bioinformatics-based screening and validation of ferroptosis-related genes in sepsis and type 2 diabetes mellitus.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- GZMA suppressed GPX4-mediated ferroptosis to improve intestinal mucosal barrier function in inflammatory bowel disease.Cell communication and signaling : CCS · 2024Article
- [Inhibitory effect of 5-hydroxy-6,7-dimethoxyflavone on H1N1 influenza virus-induced ferroptosis and inflammation in A549 cells and its possible mechanisms].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Rabeprazole suppressed gastric intestinal metaplasia through activation of GPX4-mediated ferroptosis.Frontiers in pharmacology · 2024Article
- Sorbitol Destroyed Intestinal Microfold Cells (M Cells) Development through Inhibition of PDE4-Mediated RANKL Expression.Mediators of inflammation · 2024Article
- Shikonin improves intestinal barrier function through modulation of GPX4 expression in intestinal epithelial cells.International journal of immunopathology and pharmacologyArticle
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Vitronectin (VTN) has been reported to trigger cell pyroptosis to aggravate inflammation in our previous study. However, the function of VTN in inflammatory bowel disease (IBD) remains to be addressed. Methods: Real-time PCR and western blotting were performed to analyze VTN-regulated intestinal epithelial cell (IEC) differentiation through ferroptosis, and immunofluorescence (IF), luciferase, and chromatin immunoprecipitation were used to identify whether VTN-modulated ferroptosis is dependent on phosphodiesterase 4 (PDE4)/protein kinase A (PKA)/cyclic adenosine monophosphate-response element-binding protein (CREB) cascade pathway. Results: Herein, we found that caudal-related homeobox transcription factor 2-mediated IECs differentiation was impaired in response to VTN, which was attributed to enhanced ferroptosis characterized by decreased glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 expression. Inhibition of ferroptosis in IECs rescued the inhibitory effect of VTN on cell differentiation. Further analysis showed that VTN triggered phosphorylation of PDE4, leading to inhibit PKA/CREB activation and CREB nuclear translocation, which further reduced GPX4 transactivation. Endogenous PKA interacted with CREB, and this interaction was destroyed in response to VTN stimulation. What is more, overexpression of CREB in CaCO Conclusions: These findings demonstrated that highly expressed VTN disrupted IECs differentiation through PDE4-mediated ferroptosis in IBD, suggesting targeting PDE4 could be a promising therapeutic strategy for patients with IBD.
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