ArticleInternational journal of colorectal disease2008
Inflammation modulates fibronectin isoform expression in colonic lamina propria fibroblasts (CLPF).
Article in International journal of colorectal disease, 2008. 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, 19 citations in OpenAlex.
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- Methods for Mitochondrial DNA Damage and Depletion in Immortalized Trabecular Meshwork Cells.International journal of molecular sciences · 2025Article
- Newt cells secrete extracellular vesicles with therapeutic bioactivity in mammalian cardiomyocytes.Journal of extracellular vesicles · 2018Article
- Impact of Intestinal Ultrasound on Classification and Management of Crohn's Disease Patients with Inconclusive Colonoscopy.Canadian journal of gastroenterology & hepatology · 2016Article
- Short- and long-term efficacy of endoscopic balloon dilation in Crohn's disease strictures.World journal of gastroenterology · 2013Article
- Stromal cells in the human gut show ultrastructural features of fibroblasts and smooth muscle cells but not myofibroblasts.Journal of cellular and molecular medicine · 2011Article
- Comparison of strictureplasty and endoscopic balloon dilatation for stricturing Crohn's disease--review of the literature.International journal of colorectal disease · 2010Review
- Lipid alterations in experimental murine colitis: role of ceramide and imipramine for matrix metalloproteinase-1 expression.PloS one · 2009Article
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMigration of colonic lamina propria fibroblasts (CLPF) plays an important role during mucosal wound healing as well as fibrosis and fistula formation in Crohn's disease (CD). Recently, we showed that the migratory potential of CD-CLPF was significantly reduced compared to control CLPF. Fistula-derived CD-CLPF migrated less and fibrosis-CLPF more than CLPF from inflamed CD mucosa. These changes in migratory behavior were associated with changes in production of the migration-inducing fibronectin (FN) isoforms ED-A and ED-B. A permanent reduction of the migratory potential of CLPF was mediated by IFN-gamma and tumor necrosis factor (TNF) modulate FN isofom expression in CLPF and thereby might regulate CLPF migration. MATERIALS AND
methodsControl CLPF were incubated for 72 h with IFN-gamma, TNF, IFN-gamma plus TNF, or TGF-beta1. Messenger RNA (mRNA) was isolated and expression of FN and isoforms ED-A and ED-B was quantified by real-time polymerase chain reaction. FN, ED-A, and ED-B were investigated by Western blotting. FN receptor integrin alpha5beta1 was analyzed by FACS.
resultsNo difference was found for the surface display of integrin alpha5beta1 between stimulated and non-stimulated cells. In TGF-beta1 incubated CLPF mRNA amount of FN and isoforms ED-A and ED-B was slightly increased. IFN-gamma only decreased FN in CLPF, TNF significantly reduced FN-mRNA by 40%, FN ED-A mRNA by 25%, and ED-B mRNA by 50%. The TNF-mediated mRNA downregulation resulted in a decreased protein amount as revealed by Western blotting.
conclusionCytokines such as IFN-gamma, TNF, and TGF-beta1 modulate the production of fibronectin isoforms. Our data indicate that inflammation-induced modulation of FN-isoform production is involved in the alterations of migratory potential of CLPF isolated from CD mucosa.
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