ArticleInflammatory bowel diseases2011
Endogenous IGFBP-3 regulates excess collagen expression in intestinal smooth muscle cells of Crohn's disease strictures.
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 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Gut Microbiota as a Mediator Between Intestinal Fibrosis and Creeping Fat in Crohn's Disease.United European gastroenterology journal · 2025Review
- Role of IGFBP-3 in Human Diseases Relying on Different Cell Signaling Pathways.Advanced biomedical research · 2025Review
- Comparative transcriptomic analysis validates iPSC derived in-vitro progressive fibrosis model as a screening tool for drug discovery and development in systemic sclerosis.Scientific reports · 2024Article
- Signaling Pathways of the Insulin-like Growth Factor Binding Proteins.Endocrine reviews · 2023Article
- Transcriptome profiling of intact bowel wall reveals that PDE1A and SEMA3D are possible markers with roles in enteric smooth muscle apoptosis, proliferative disorders, and dysautonomia in Crohn's disease.Frontiers in genetics · 2023Article
- Colon stroma mediates an inflammation-driven fibroblastic response controlling matrix remodeling and healing.PLoS biology · 2022Article
- Malnourishment affects gene expression along the length of the small intestine.Frontiers in nutrition · 2022Article
- Association of DNA Methylation in Blood Pressure-Related Genes With Ischemic Stroke Risk and Prognosis.Frontiers in cardiovascular medicine · 2022Article
- Upregulated IGFBP3 with Aging Is Involved in Modulating Apoptosis, Oxidative Stress, and Fibrosis: A Target of Age-Related Erectile Dysfunction.Oxidative medicine and cellular longevity · 2022Article
- Mechanism of fibrosis and stricture formation in Crohn's disease.Scandinavian journal of immunology · 2020Review
- Immunological roles of intestinal mesenchymal cells.Immunology · 2020Review
- Review
- Epithelial-stromal crosstalk and fibrosis in eosinophilic esophagitis.Journal of gastroenterology · 2019Review
- Microvesicle-mediated delivery of miR-1343: impact on markers of fibrosis.Cell and tissue research · 2018Article
- ATP-mediated Events in Peritubular Cells Contribute to Sterile Testicular Inflammation.Scientific reports · 2018Article
- Increased IGF-IEc expression and mechano-growth factor production in intestinal muscle of fibrostenotic Crohn's disease and smooth muscle hypertrophy.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Noncanonical STAT3 activation regulates excess TGF-β1 and collagen I expression in muscle of stricturing Crohn's disease.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Contribution of intestinal smooth muscle to Crohn's disease fibrogenesis.European journal of histochemistry : EJH · 2014Article
- Mechanisms that mediate the development of fibrosis in patients with Crohn's disease.Inflammatory bowel diseases · 2014Review
- Serum concentrations of insulin-like growth factor-binding protein 5 in Crohn's disease.World journal of gastroenterology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundStricture formation occurs in ≈30% of patients with Crohn's disease (CD) and is a significant cause of morbidity. Strictures are characterized by intestinal smooth muscle cell hyperplasia, smooth muscle cell hypertrophy, and fibrosis due to excess net extracellular matrix production, including collagen. Transforming growth factor-β1 (TGF-β1) has profibrotic effects in many tissues due to its ability to regulate collagen expression and extracellular matrix dynamics. We previously showed that both insulin-like growth factor (IGF) binding protein-3 (IGFBP-3) and TGF-β1 are expressed by normal human intestinal smooth muscle cells, bind to, and activate TGF-βRII/I receptors in these cells.
methodsSmooth muscle cells isolated from the muscularis propria of patients were used to prepare RNA, protein lysates, or placed into primary culture. IGFBP-3, TGF-β1, and collagen IαI expression was measured with quantitative reverse-transcription polymerase chain reaction (RT-PCR) and protein levels by enzyme-linked immunosorbent assay (ELISA) or immunoblot.
resultsExpression and production of IGFBP-3, TGF-β1, and collagen IαI were significantly increased specifically in smooth muscle cells isolated from regions of strictured intestine in CD compared to nonstrictured histologically normal resection margin. IGFBP-3 and TGF-β1 regulated collagen IαI expression and production via a TGF-βRII/I-dependent and Smad2/3-dependent mechanism. Upregulated (excess) collagen IαI expression and production in smooth muscle cells of strictures and basal collagen IαI in smooth muscle cells of normal margin were inhibited by immunoneutralization of IGFBP-3 or TGF-β1.
conclusionsThe findings indicate that upregulated endogenous IGFBP-3 and TGF-β1 expression regulates excess collagen IαI production and contributes to fibrosis and stricture formation in CD.
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