Structural-proliferative units and organ growth: effects of insulin-like growth factor 2 on the growth of colon and skin

Bennett, Bill; Crew, Tracey E.; Slack, Jonathan; Ward, Andrew

doi:10.1242/dev.00333

Cited by 35 publications

(28 citation statements)

References 41 publications

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“…Furthermore, considering the involvement of ROS scavengers on preserving NO and caveolin-1 signaling (3,9), we determined whether supplementation increases the gene expression of SOD and GPX. The key findings of our study are as follows: 1) formula feeding with and without supplementation results in significant growth restriction compared with the maternally fed controls; 2) Despite suboptimal nutrition, IGF-I, IGF-2, and EGF, which play significant roles in intestinal mucosal repair, intestinal epithelial healing, regeneration, and permeability (23)(24)(25)(26)(27), were increased in the neonatal rat ileum; 3) caveolin-1, eNOS, and nNOS are simultaneously down-regulated with formula feeding, whereas iNOS is up-regulated. Supplementation did not reverse this effect; 4) SOD-2, SOD-3, and copper chaperone for SOD were down-regulated with formula feeding, an effect that remained sustained with supplementation.…”

Section: Discussionmentioning

confidence: 80%

Effects of Probiotics, Prebiotics, and Synbiotics on Messenger RNA Expression of Caveolin-1, NOS, and Genes Regulating Oxidative Stress in the Terminal Ileum of Formula-Fed Neonatal Rats

et al. 2010

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Necrotizing enterocolitis (NEC) afflicts extremely low birth weight neonates, and probiotics reduces its incidence and severity. NO is involved in the pathogenesis of NEC, and caveolin-1 regulates NO signaling. We tested the hypothesis that intestinal caveolin-1 and NOS are deficient in formula-fed neonatal rats and that supplementation with "Florastar Kids" and/or galactooligosaccharides and fructo-oligosaccharides preserves caveolin-1 and NOS. At birth (P0), neonatal rat pups were maternally fed or hand-gavaged with or without supplemented formula. Samples from the terminal ileum were analyzed for total NO metabolites, growth factors, and gene expression of caveolin-1, NOS isoforms, and antioxidants. Our data showed that formula feeding with and without supplementation resulted in significant growth restriction. Despite suboptimal nutrition, growth factors involved in intestinal repair and regeneration were increased in the neonatal rat ileum. Caveolin-1, endothelial NOS, and neuronal NOS were simultaneously downregulated with formula feeding while inducible NOS was upregulated. Superoxide dismutase and glutathione peroxidase were up-regulated with supplementation. These data provide a probable mechanism for the benefits of supplemented formula for decreasing the severity of NEC by preserving the antioxidant systems. (Pediatr Res 67: 526-531, 2010)

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Section: Discussionmentioning

confidence: 80%

Effects of Probiotics, Prebiotics, and Synbiotics on Messenger RNA Expression of Caveolin-1, NOS, and Genes Regulating Oxidative Stress in the Terminal Ileum of Formula-Fed Neonatal Rats

et al. 2010

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“…Overall, this suggests that Igf2 has predominant effects on adenoma progression when compared at a single time point (120 days), which seem to become more marked with increasing time. 3 Here, we cannot exclude modifier effects on adenoma initiation during crypt fission events in early intestinal development (42). A, ratio of villus to crypt epithelial nuclei number (height) in the proximal, middle, and distal thirds of the small intestine.…”

Section: Igf2mentioning

confidence: 98%

Soluble IGF2 Receptor Rescues Apc Min/+ Intestinal Adenoma Progression Induced by Igf2 Loss of Imprinting

et al. 2006

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The potent growth-promoting activity of insulin-like growth factor-II (IGF-II) is highly regulated during development but frequently up-regulated in tumors. Increased expression of the normally monoallelic (paternally expressed) mouse (Igf2) and human (IGF2) genes modify progression of intestinal adenoma in the Apc Min/+ mouse and correlate with a high relative risk of human colorectal cancer susceptibility, respectively. We examined the functional consequence of Igf2 allelic dosage (null, monoallelic, and biallelic) on intestinal adenoma development in the Apc Min/+ by breeding with mice with either disruption of Igf2 paternal allele or H19 maternal allele and used these models to evaluate an IGF-II-specific therapeutic intervention. Increased allelic Igf2 expression led to elongation of intestinal crypts, increased adenoma growth independent of systemic growth, and increased adenoma nuclear B-catenin staining. By introducing a transgene expressing a soluble form of the full-length IGF-II/mannose 6-phosphate receptor (sIGF2R) in the intestine, which acts as a specific inhibitor of IGF-II ligand bioavailability (ligand trap), we show rescue of the Igf2-dependent intestinal and adenoma phenotype. This evidence shows the functional potency of allelic dosage of an epigenetically regulated gene in cancer and supports the application of an IGF-II ligand-specific therapeutic intervention in colorectal cancer. (Cancer Res 2006; 66(4): 1940-8)

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“…Instead, Grb10 acts within a separate growth axis in a manner consistent with the parent-offspring conflict hypothesis genomic sequence deleted from the Grb10⌬2-4 allele (MP11F 5Ј-AGCCCATGTGCTGTCTTTCT-3Ј and MP11R 5Ј-AGGGA-CAGACGGTTCAGAGA-3Ј). Igf2⌬ mice (19) were maintained for several generations on the same mixed C57BL͞6:CBA genetic background and were genotyped by using a PCR assay described previously (20). All mice were housed under the standard conditions given previously (20).…”

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confidence: 99%

“…Igf2⌬ mice (19) were maintained for several generations on the same mixed C57BL͞6:CBA genetic background and were genotyped by using a PCR assay described previously (20). All mice were housed under the standard conditions given previously (20).…”

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confidence: 99%

Disruption of the imprinted Grb10 gene leads to disproportionate overgrowth by an Igf2-independent mechanism

Charalambous

Smith

Bennett

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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257

275

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To investigate the function of the Grb10 adapter protein, we have generated mice in which the Grb10 gene was disrupted by a gene-trap insertion. Our experiments confirm that Grb10 is subject to genomic imprinting with the majority of Grb10 expression arising from the maternally inherited allele. Consistent with this, disruption of the maternal allele results in overgrowth of both the embryo and placenta such that mutant mice are at birth Ϸ30% larger than normal. This observation establishes that Grb10 is a potent growth inhibitor. In humans, GRB10 is located at chromosome 7p11.2-p12 and has been associated with Silver-Russell syndrome, in which Ϸ10% of those affected inherit both copies of chromosome 7 from their mother. Our results indicate that changes in GRB10 dosage could, in at least some cases, account for the severe growth retardation that is characteristic of Silver-Russell syndrome. Because Grb10 is a signaling protein capable of interacting with tyrosine kinase receptors, we tested genetically whether Grb10 might act downstream of insulin-like growth factor 2, a paternally expressed growth-promoting gene. The result indicates that Grb10 action is essentially independent of insulinlike growth factor 2, providing evidence that imprinting acts on at least two major fetal growth axes in a manner consistent with parent-offspring conflict theory.adapter protein ͉ cell signaling ͉ genomic imprinting ͉ growth factor receptor-bound protein ͉ insulin-like growth factor

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Structural-proliferative units and organ growth: effects of insulin-like growth factor 2 on the growth of colon and skin

Cited by 35 publications

References 41 publications

Effects of Probiotics, Prebiotics, and Synbiotics on Messenger RNA Expression of Caveolin-1, NOS, and Genes Regulating Oxidative Stress in the Terminal Ileum of Formula-Fed Neonatal Rats

Effects of Probiotics, Prebiotics, and Synbiotics on Messenger RNA Expression of Caveolin-1, NOS, and Genes Regulating Oxidative Stress in the Terminal Ileum of Formula-Fed Neonatal Rats

Soluble IGF2 Receptor Rescues Apc Min/+ Intestinal Adenoma Progression Induced by Igf2 Loss of Imprinting

Disruption of the imprinted Grb10 gene leads to disproportionate overgrowth by an Igf2-independent mechanism

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