ArticleJournal of pediatric surgery2013
IGF-2 mediates intestinal mucosal hyperplasia in retinoblastoma protein (Rb)-deficient mice.
Article in Journal of pediatric surgery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Enteral delivery of proteins enhances the expression of proteins involved in the cytoskeleton and protein biosynthesis in human duodenal mucosa.The American journal of clinical nutrition · 2015Trial
- Article
- Host-Gut Microbiota Crosstalk in Intestinal Adaptation.Cellular and molecular gastroenterology and hepatology · 2018Review
- Epithelial IGF1R is dispensable for IGF2 mediated enhanced intestinal adaptation in retinoblastoma-deficient mice.Journal of pediatric surgery · 2017Article
- The Pathogenesis of Resection-Associated Intestinal Adaptation.Cellular and molecular gastroenterology and hepatology · 2016Review
- Mechanisms of intestinal adaptation.Best practice & research. Clinical gastroenterology · 2016Review
- High-protein diet improves postoperative weight gain after massive small-bowel resection.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2015Article
- IGF-2 is necessary for retinoblastoma-mediated enhanced adaptation after small-bowel resection.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2014Article
- Insulin-like growth factor 2 and its enterocyte receptor are not required for adaptation in response to massive small bowel resection.Journal of pediatric surgery · 2014Article
- Glucose transporter 8 (GLUT8) mediates fructose-induced de novo lipogenesis and macrosteatosis.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purposeWe have previously demonstrated a hyperplastic phenotype when Rb expression was disrupted within the intestinal epithelium. These findings mimic resection-induced adaptation suggesting a possible mechanistic role for Rb during adaptation. The purpose of the present study was to elucidate a mechanism for how Rb deficiency induces intestinal hyperplasia.
methodsEnterocytes isolated from intestine-specific Rb knockout mice (Rb-IKO) underwent a microarray to elucidate their gene expression profile. IGF2 expression was significantly elevated, which was subsequently confirmed by RT-PCR and in situ mRNA hybridization. Mice with deficient expression of IGF2 or its receptor IGF1R were therefore crossed with Rb-IKO mice to determine the significance of IGF2 in mediating the Rb-IKO intestinal phenotype.
resultsExpression of IGF2 was significantly elevated in villus enterocytes of Rb-IKO mice. The mucosal hyperplasia in Rb-IKO mice was reversed when either IGF2 or IGF1R expression was genetically disrupted in Rb-IKO mice.
conclusionIGF-2 expression is significantly elevated in villus enterocytes and is required for the hyperplastic intestinal mucosal phenotype of Rb-IKO mice. The trophic effects of IGF2 require intact IGF1R signaling within the intestinal epithelium. These findings reveal novel regulatory roles for Rb in expanding intestinal mucosal surface area.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.