ArticleBritish journal of pharmacology2014
PDGF and TGF-β promote tenascin-C expression in subepithelial myofibroblasts and contribute to intestinal mucosal protection in mice.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Genetic background influences developmental airway smooth muscle program and susceptibility to airway hyperresponsiveness in mice.JCI insight · 2026Article
- A spatial and temporal transcriptomic atlas of mouse intestinal regeneration in the jejunum.Nature communications · 2026Article
- Association ofInternational journal of molecular sciences · 2026Article
- Article
- Dietary lecithin attenuates adverse effects of high fat diet on antioxidant activity, inflammation and fibrotic damage in the kidney of blunt snout bream (Megalobrama amblycephala).Fish physiology and biochemistry · 2026Article
- Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice.bioRxiv : the preprint server for biology · 2025Article
- The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Villus myofibroblasts are developmental and adult progenitors of mammalian gut lymphatic musculature.Developmental cell · 2024Article
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
- Imaging the Alternatively Spliced D Domain of Tenascin C in a Preclinical Model of Inflammatory Bowel Disease.Molecular imaging and biology · 2023Article
- Tenascin-C is a driver of inflammation in the DSS model of colitis.Matrix biology plus · 2022Article
- Investigating the development of diarrhoea through gene expression analysis in sheep genetically resistant to gastrointestinal helminth infection.Scientific reports · 2022Article
- Role of Extracellular Matrix in Gastrointestinal Cancer-Associated Angiogenesis.International journal of molecular sciences · 2020Review
- AGAP2: Modulating TGFβ1-Signaling in the Regulation of Liver Fibrosis.International journal of molecular sciences · 2020Review
- Stromal integrin α11 regulates PDGFR-β signaling and promotes breast cancer progression.The Journal of clinical investigation · 2019Article
- Tenascin-C expression contributes to pediatric brainstem glioma tumor phenotype and represents a novel biomarker of disease.Acta neuropathologica communications · 2019Article
- Tenascin-C Is Increased in Inflammatory Bowel Disease and Is Associated with response to Infliximab Therapy.BioMed research international · 2019Article
- Induction of myosin light chain kinase and CPI-17 by TGF-β accelerates contractile activity in intestinal epithelial cells.The Journal of veterinary medical science · 2018Article
- Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeTenascin-C (TnC) is a multi-domain extracellular matrix glycoprotein that is expressed at a high level during embryogenesis but is almost absent during normal postnatal life. This multi-domain complex molecule is reported to associate with both pro-inflammatory and anti-inflammatory signalling cascades. In this study, we examined how TnC modulated intestinal inflammation. EXPERIMENTAL APPROACH: TnC pathophysiology was evaluated in cultures of rat intestinal subepithelial myofibroblasts (ISEMF) and intestinal epithelial cells. Wild-type and TnC(-/-) mice were treated with dextran sodium sulfate (DSS) to induce colitis. KEY
resultsDSS-induced colitis in mice markedly increased TnC in the damaged mucosal areas and up-regulated mRNA for TnC, pro-inflammatory cytokines and growth factors (PDGF-B and TGF-β1). In addition, 2,4,6-trinitrobenzene sulfonic acid-induced colitis and SAMP1/Yit mice, a model of spontaneous Crohn's disease, also exhibited increased mucosal TnC in colon and ilea respectively. PDGF receptor-α (PDGFRα) positive ISEMF were the primary TnC-producing cells in colon tissues. Accordingly, ISEMF collected from the rat colon constitutively expressed both TnC and PDGFRα. PDGF-BB and TGF-β1 up-regulated both TnC mRNA and protein levels in ISEMF. Knock-down of TnC gene increased susceptibility to DSS-induced colitis, compared with TnC(+/+) littermates. TnC(-/-) mice showed marked abrasion of intestinal mucosal barrier and increased inflammatory scores. Moreover, TnC accelerated both trans-well migration and wound healing in epithelial cells. CONCLUSIONS AND IMPLICATIONS: The pharmacological profiles of PDGF-BB and TGF-β in colitis tissues and ISEMF suggest that increased TnC production during inflammation contributed to epithelial cell migration, remodelling and protection of intestinal barriers.
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