ArticleInflammatory bowel diseases2011
Amelioration of excess collagen IαI, fibrosis, and smooth muscle growth in TNBS-induced colitis in IGF-I(+/-) mice.
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 19 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Pooled it
- Insights into the Molecular Mechanisms and Novel Therapeutic Strategies of Stenosis Fibrosis in Crohn's Disease.Biomedicines · 2025Review
- Intestinal fibrosis associated with inflammatory bowel disease: Known and unknown.Chinese medical journal · 2025Review
- Pitavastatin reduces intestinal fibrosis in chronic colitis and inhibits colon fibroblast activation by enhancing MMP-9 expression via the IGF-1/IGF-1R pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- Mesenchymal Stem/Stromal Cells in Progressive Fibrogenic Involvement and Anti-Fibrosis Therapeutic Properties.Frontiers in cell and developmental biology · 2022Review
- Non-invasive evaluation of intestinal disorders: The role of elastographic techniques.World journal of gastroenterology · 2017Review
- Collagen and heparan sulfate coatings differentially alter cell proliferation and attachmentTechnology · 2016Article
- 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
- Mechanisms that mediate the development of fibrosis in patients with Crohn's disease.Inflammatory bowel diseases · 2014Review
- Medical therapy of stricturing Crohn's disease: what the gut can learn from other organs - a systematic review.Fibrogenesis & tissue repair · 2014Article
- Inflammatory cytokines promote growth of intestinal smooth muscle cells by induced expression of PDGF-Rβ.Journal of cellular and molecular medicine · 2014Article
- Anorectal physiology and pathophysiology in the elderly.Clinics in geriatric medicine · 2014Review
- Increased activation of latent TGF-β1 by αVβ3 in human Crohn's disease and fibrosis in TNBS colitis can be prevented by cilengitide.Inflammatory bowel diseases · 2013Article
- Article
- Animal models of intestinal fibrosis: new tools for the understanding of pathogenesis and therapy of human disease.American journal of physiology. Gastrointestinal and liver physiology · 2012Review
- Insulin-like growth factors in the gastrointestinal tract and liver.Endocrinology and metabolism clinics of North America · 2012Review
- Insulin-like growth factor 1: common mediator of multiple enterotrophic hormones and growth factors.Current opinion in gastroenterology · 2012Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundStrictures occur in ≈ 30% of patients with Crohn's disease (CD) and are characterized by intestinal smooth muscle hyperplasia, hypertrophy, and fibrosis due to excess extracellular matrix production including collagen. Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis. While upregulated IGF-I is conjectured to cause smooth muscle cell growth and collagen production in the inflamed intestine, its role in the development of fibrosis has not been directly demonstrated.
methodsColitis was induced in IGF-I(+/-) or wildtype C57BL/6J mice by rectal administration of TNBS or ethanol vehicle. After 7 days, colonic smooth muscle cells were isolated and used to prepare RNA or protein lysates. Transcript levels of IGF-IEa, IGF binding protein (IGFBP)-3, IGFBP-5, TGF-β1, and collagen IαI were measured by quantitative reverse-transcription polymerase chain reaction (RT-PCR). Corresponding protein levels were measured by Western blot or enzyme-linked immunosorbent assay (ELISA). Fibrosis was measured using digital image analysis of Masson's trichrome-stained histologic sections.
resultsIn IGF-I(+/-) mice, which express significantly lower levels of IGF-I than wildtype, the response to TNBS-induced colitis: upregulation of IGF-I, IGFBP-3, IGFBP-5 muscle growth, and collagen IαI expression, the resulting collagen deposition, and fibrosis are all significantly diminished compared to C57BL/6J wildtype controls. TGF-β1 expression and its increase following TNBS administration are not altered in IGF-I(+/-) mice compared to wildtype.
conclusionsThe findings indicate that IGF-I is a key regulator in intestinal smooth muscle hyperplasia and excess collagen production that leads to fibrosis and long term to stricture formation.
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Registered trials
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