Identification and<i>in Situ</i>Localization of the Insulin-Like Growth Factor-II/Mannose-6-Phosphate (IGF-II/M6P) Receptor in the Rat Gastrointestinal Tract: Comparison with the IGF-I Receptor*

Heinz‐Erian, Peter; Kessler, Ulrike; Funk, B.; Gais, Peter; Kieß, Wieland

doi:10.1210/endo-129-4-1769

Cited by 71 publications

(32 citation statements)

References 28 publications

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“…The presence of both type I and II IGF receptors throughout the gastrointestinal tract has been confirmed in rats and localized to both mucosal and muscularis layers [78], suggesting that exogenous IGFs may be able to interact with the intestine and elicit physiological responses.…”

Section: Insulin-like Growth Factormentioning

confidence: 92%

Growth factors from bovine milk and colostrum: composition, extraction and biological activities

Gauthier

Pouliot

Maubois

2006

Lait

125

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-EGF, BTC, IGF-I, IGF-II, TGF-β1, TGF-β2, FGF1 and 2, and PDGF are the main growth factors present in bovine milk and colostrum. All of these growth factors are also found in human milk but at a lower concentration. The various compositional data reported in the literature vary greatly but it is evidenced that the day of lactation has the most important effect. Milk growth factors are characterized by a neutral to alkaline isoelectric point (pI) and a molecular mass between 6400 g·mol -1 and 30000 g·mol -1 . However, many of the growth factors are in a latent form, bound to high-molecular-mass proteins. Milk growth factors are resistant generally to pasteurization but disulfide reducing agents have been found to inactivate some species such as TGF-β's. The published data on bioavailability of milk growth factors are somewhat contradictory but it is generally accepted that they are resistant to gastric digestion and they can exert local and systemic effects on the gastrointestinal tract. Cation-exchange chromatography has been widely used for the extraction of milk growth factors because of the basic nature of these molecules. Membrane separations such as microfiltration (MF) have also been used successfully for the extraction of immunoglobulins and of some growth factors from colostrum, while ultrafiltration (UF) was successful only at separating IGF-I and IGF-II in whey. Milk growth factor extracts have been developed for various applications such as treatment of gastrointestinal disorders and skin diseases, wound healing, and induction of oral tolerance.

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Section: Insulin-like Growth Factormentioning

confidence: 92%

Growth factors from bovine milk and colostrum: composition, extraction and biological activities

Gauthier

Pouliot

Maubois

2006

Lait

125

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“…In addition to EGFR, the insulin-like growth factor-1 receptor (IGF-1R) can be activated by its cognate ligand IGF-1 and transactivated in response to GPCR ligands such as thrombin (30) and angiotensin II (31). IGF-1R is expressed in human intestinal smooth muscle cells (32), cells of the muscularis propria, and the intestinal mucosa (33). IGF-1 regulates gastrointestinal tract growth and tissue repair as well as tumorigenesis through binding to its high-affinity receptor IGF-1R, which activates a number of signaling transduction pathways, including PI3K and downstream kinase Akt (34).…”

Section: Neurotensin (Nt)mentioning

confidence: 99%

Insulin-like Growth Factor-1 Receptor Transactivation Modulates the Inflammatory and Proliferative Responses of Neurotensin in Human Colonic Epithelial Cells

Zhao

Bakirtzi

Zhan

et al. 2011

Journal of Biological Chemistry

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sion. This is the first report to indicate that NT transactivates IGF-1R and that this response is linked to Akt phosphorylation and NF-B activation, contributing to both pro-inflammatory and tissue repair signaling pathways in response to NT in colonic epithelial cells. We propose that IGF-1R activation represents a previously unrecognized key pathway involved in the mechanisms by which NT and NTR1 modulate colonic inflammation and inflammatory bowel disease. Neurotensin (NT)4 is a 13-amino acid neuropeptide initially isolated from the bovine hypothalamus by Carraway and Leeman (1) and is highly expressed in the gastrointestinal tract (2). NT modulates motility in the stomach, small bowel, and colon (3-5) and stimulates secretion in the dog jejunum (6) and human colonic mucosa (7,8). NT also stimulates growth and regeneration of the intestinal mucosa (9, 10) and has been implicated in the pathophysiology of colon cancer (11,12).Two G-protein-coupled receptors (GPCRs) have been described for NT: a high-affinity (NTR1) and a low-affinity (NTR2) receptor (13). A third, non-GPCR has also been identified (14). Several studies underlined the importance of NTR1 in several intestinal pathologic conditions. Administration of the specific NTR1 antagonist SR 48692 to rats inhibits colonic responses to stress (15, 16) and reduces colonic secretion and inflammation mediated by Clostridium difficile toxin A (17). Increased NTR1 expression is evident in the colonic mucosa during the course of acute colitis mediated by toxin A (17), in the colons of mice with experimental colitis (18), and in humans with inflammatory bowel disease (18). In a recent study, we also showed that involvement of NT in colonic inflammation may include direct stimulation of pro-inflammatory chemoattractant IL-8 transcription in colonic epithelial cells (19).NT stimulates several intracellular signaling events, as shown in human colonic and pancreatic cell lines expressing endogenous NTR1 (20, 21). These include increased intracellular calcium release (22, 23) and activation of the MAPK family member ERK1/2 in pancreatic MIA PaCa-2 cells (24), transformed colonic adenocarcinoma HT29 cells (24), and non-transformed human colonic epithelial NCM460 cells (19). Our recent studies indicate that NT also activates the NF-B pathway (19) and the Rho family of small GTPases (25,26). Two previous studies showed that pretreatment with PKC inhibitors reduces NT-induced ERK1/2 activation in CHO cells overexpressing NTR1 (24) and in pancreatic carcinoma PANC-1 cells expressing endogenous NTR1 (27). In contrast, our laboratory and Hassan et al. have found that EGF receptor (EGFR) transactivation is involved in NT-in-

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“…Colonic epithelial cells possess insulin, IGF-1, IGF-2, and leptin receptors (10,11). In addition, the insulin and IGF receptors are present at greater levels in tumors compared with normal colonic epithelium (12).…”

Section: Introductionmentioning

confidence: 99%

Leptin, Insulin-Like Growth Factor-1, and Insulin-Like Growth Factor-2 Are Mitogens in ApcMin/+ but not Apc+/+ Colonic Epithelial Cell Lines

Fenton

Hord

Lavigne

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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The obese state is associated with elevated circulating levels of insulin, insulin-like growth factors (IGF), and leptin. Research is contradictory regarding the role of these elevated growth factors in colon cancer risk. We hypothesized that colonic epithelial cells that were Apc deficient (Apc Min/+ ) but not those expressing wild-type Apc (Apc +/+ ) would experience a hyperproliferative and antiapoptotic phenotype when exposed to these growth factors. This hypothesis was addressed using two nontumorigenic murine colonic epithelial cell lines with distinct Apc genotypes: Apc +/+ YAMC cells and Apc Min/+ IMCE cells. Cells were treated for 48 hours with various concentrations of leptin (0.001-50 ng/mL), IGF-1 (0.1-200 ng/mL), or IGF-2 (0.1-600 ng/mL). In YAMC cells, leptin caused a significant decrease in cell proliferation (P < 0.01) compared with controls due to induction of caspase activity and apoptosis. In contrast, in the IMCE cells, leptin induced a 75% increase in cell proliferation compared with controls (P < 0.0001). IGF-1 and IGF-2 also induced 50% greater proliferation in the IMCE cells (P < 0.001) compared with controls. Cotreatment of IMCE cells with leptin and either IGF-1 or IGF-2 induced greater proliferation than either growth factor alone (P < 0.0001). IMCE cell proliferation caused by leptin only treatment was associated with activation of p42/44 mitogen-activated protein kinase (MAPK), p38 MAPK, and nuclear factor-KB nuclear translocation but not with MAPK kinase or Janus-activated kinase/ signal transducers and activators of transcription activation. These data provide the first evidence that leptin may interact with IGFs to promote survival and expansion of colonic epithelial cells that were Apc deficient (Apc Min/+ ) but not those expressing wild-type Apc (Apc +/+ ). (Cancer Epidemiol Biomarkers Prev 2005;14(7):1646 -52)

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Identification andin SituLocalization of the Insulin-Like Growth Factor-II/Mannose-6-Phosphate (IGF-II/M6P) Receptor in the Rat Gastrointestinal Tract: Comparison with the IGF-I Receptor*

Cited by 71 publications

References 28 publications

Growth factors from bovine milk and colostrum: composition, extraction and biological activities

Growth factors from bovine milk and colostrum: composition, extraction and biological activities

Insulin-like Growth Factor-1 Receptor Transactivation Modulates the Inflammatory and Proliferative Responses of Neurotensin in Human Colonic Epithelial Cells

Leptin, Insulin-Like Growth Factor-1, and Insulin-Like Growth Factor-2 Are Mitogens in ApcMin/+ but not Apc+/+ Colonic Epithelial Cell Lines

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