ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Endogenous IGF-I and alpha v beta3 integrin ligands regulate increased smooth muscle growth in TNBS-induced colitis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Intestinal fibrosis: ready to be reversed.Current opinion in gastroenterology · 2017Review
- Collagen and heparan sulfate coatings differentially alter cell proliferation and attachmentTechnology · 2016Article
- 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
- Forkhead box F2 regulation of platelet-derived growth factor and myocardin/serum response factor signaling is essential for intestinal development.The Journal of biological chemistry · 2015Article
- Cytokine-induced S-nitrosylation of soluble guanylyl cyclase and expression of phosphodiesterase 1A contribute to dysfunction of longitudinal smooth muscle relaxation.The Journal of pharmacology and experimental therapeutics · 2015Article
- Cytokine-induced iNOS and ERK1/2 inhibit adenylyl cyclase type 5/6 activity and stimulate phosphodiesterase 4D5 activity in intestinal longitudinal smooth muscle.American journal of physiology. Cell physiology · 2014Article
- Hypercontractility of intestinal longitudinal smooth muscle induced by cytokines is mediated by the nuclear factor-κB/AMP-activated kinase/myosin light chain kinase pathway.The Journal of pharmacology and experimental therapeutics · 2014Article
- Jun kinase-induced overexpression of leukemia-associated Rho GEF (LARG) mediates sustained hypercontraction of longitudinal smooth muscle in inflammation.American journal of physiology. Cell physiology · 2014Article
- Resveratrol inhibits collagen I synthesis by suppressing IGF-1R activation in intestinal fibroblasts.World journal of gastroenterology · 2014Article
- Changes in the expression of smooth muscle contractile proteins in TNBS- and DSS-induced colitis in mice.Inflammation · 2013Article
- 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
- IL-33-induced alterations in murine intestinal function and cytokine responses are MyD88, STAT6, and IL-13 dependent.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Mechanisms of smooth muscle responses to inflammation.Neurogastroenterology and motility · 2012Review
- Osteopontin ablation attenuates progression of colitis in TNBS model.Digestive diseases and sciences · 2012Article
- Amelioration of excess collagen IαI, fibrosis, and smooth muscle growth in TNBS-induced colitis in IGF-I(+/-) mice.Inflammatory bowel diseases · 2011Article
- Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endogenous insulin-like growth factor-I (IGF-I) regulates intestinal smooth muscle growth by concomitantly stimulating proliferation and inhibiting apoptosis. IGF-I-stimulated growth is augmented by the alpha(v)beta(3) integrin ligands vitronectin and fibronectin. IGF-I expression in smooth muscle is increased in both TNBS-induced colitis and Crohn's disease. We hypothesized that intestinal inflammation increased vitronectin and fibronectin expression by smooth muscle and, along with IGF-I upregulation, increased intestinal muscle growth. Intestinal smooth muscle cells were examined 7 days following the induction of TNBS-induced colitis. Although alpha(v)beta(3) integrin expression was not altered by TNBS-induced colitis, vitronectin and fibronectin levels were increased by 80 +/- 10% and 90 +/- 15%, above control levels, respectively. Basal IGF-I receptor phosphorylation in inflamed muscle from TNBS-treated rats was increased by 86 +/- 8% over vehicle-treated controls. Basal ERK1/2, p70S6 kinase, and GSK-3beta phosphorylation in muscle cells of TNBS-treated rats were also increased by 140-180%. TNBS treatment increased basal muscle cell proliferation by 130 +/- 15% and decreased apoptosis by 20 +/- 2% compared with that in vehicle-treated controls. The changes in proliferation and apoptosis were reversed by an IGF-I receptor tyrosine kinase inhibitor or an alpha(v)beta(3) integrin antagonist. The results suggest that smooth muscle hyperplasia in TNBS-induced colitis partly results from the upregulation of endogenous IGF-I and ligands of alpha(v)beta(3) integrin that mediate increased smooth muscle cell proliferation and decreased apoptosis. This paper has identified one mechanism regulating smooth muscle hyperplasia, a feature of stricture formation that occurs in the chronically inflamed intestine of TNBS-induced colitis and potentially Crohn's disease.
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