Insulinlike growth factor I and interleukin 1β messenger RNA in a rat model of granulomatous enterocolitis and hepatitis

Zimmermann, Ellen M.; Sartor, R. Balfour; McCall, Robert Donnell; Pardo, M. J. Cruces; Bender, Diane; Lund, P. Kay

doi:10.1016/0016-5085(93)90713-m

Cited by 86 publications

(75 citation statements)

References 34 publications

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“…Its is known that normal hepatocytes express few IGF-I receptors, and that growth of normal liver is not affected by circulating IGF-I [11,48,49]. In agreement with this, we have not detected the expression of IGF-I receptors in total liver homogenates of CO, CI nor healthy control rats treated with IGF-I, when analysed by Western blotting (data not shown).…”

Section: Discussionsupporting

confidence: 88%

“…The hepatoprotective action of IGF-I in this experimental model can be attributed in part to its ability to modulate the peroxidative liver damage elicited by CCl 4 [10]. However, the molecular mechanisms behind this in vivo effect of IGF-I are not completely known, and can be further complicated by the fact that hepatic parenchymal cells express few IGF-I receptors [11].…”

Section: Introductionmentioning

confidence: 93%

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Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Mirpuri

Garcı́a-Trevijano

Castilla‐Cortázar

et al. 2002

The International Journal of Biochemistry & Cell Biology

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We have previously shown that the administration of low doses of insulin-like growth factor-I (IGF-I) to CCl 4 -cirrhotic rats improves liver function and reduces fibrosis. To better understand the mechanisms behind the hepatoprotective effects of IGF-I, and to identify those genes whose expression is affected in cirrhosis and after IGF-1 treatment, we have performed differential display of mRNA analysis by means of polymerase chain reaction (PCR) in livers from control and CCl 4 -cirrhotic rats treated or not with IGF-I. We have identified 16 genes that were up-or down-regulated in the cirrhotic liver. IGF-I treatment partially normalized the expression of eight of these genes, including serine proteinase inhibitors such as serpin-2 and alpha-1-antichymotripsin, alpha-1-acid glycoprotein, and alpha-2u-globulin. Additionally, we show that IGF-I enhanced the regenerative activity in the cirrhotic liver, as determined by the increased expression of the proliferating cell nuclear antigen (PCNA). Finally, IGF-I treatment partially restored the expression of growth hormone receptor (GHR) and the levels of global genomic DNA methylation, which are reduced in human and experimental cirrhosis. Taken together, our observations confirm the hepatoprotective effects of IGF-I, and suggest that this action can be exerted in part through the normalization of liver gene expression, growth hormone (GH) responsiveness and global genomic DNA methylation.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 93%

Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Mirpuri

Garcı́a-Trevijano

Castilla‐Cortázar

et al. 2002

The International Journal of Biochemistry & Cell Biology

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“…Growth factors such as PDGF-BB, basic fibroblast growth factor (bFGF), 1 and EGF are found in the colonic mucosa (4,5), and are mitogens for myofibroblast-like cells derived from other tissues. IGF-I and IGF-II have been shown to be upregulated in animal models of chronic inflammation (6) and have been shown to promote survival of other mesenchymal cells (7). The proinflammatory cytokines IL-1 ␤ (8) and TNF-␣ are upregulated in inflammation of the colon (9), and are thought to play a key role in initiating the inflammatory response (10).…”

Section: Introductionmentioning

confidence: 99%

Regulation of proliferation of human colonic subepithelial myofibroblasts by mediators important in intestinal inflammation.

Jobson

Billington²,

Hall³

1998

J. Clin. Invest.

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An increase in myofibroblast number may be necessary for wound healing but may also lead to postinflammatory scarring. We have, therefore, studied the role of mediators important in inflammatory bowel disease in regulating proliferation of human colonic myofibroblasts. Using primary cultures of these cells, we have shown increases in [ 3 H]thymidine incorporation in response to platelet-derived growth factor (EC 50 ϭ 14 ng/ml), basic fibroblast growth factor (EC 50 ϭ 2.2 ng/ml), and epidermal growth factor (EC 50 ϭ 1.1 ng/ml). Coulter counting of cell suspensions demonstrated increases in cell number with these growth factors along with insulin-like growth factor-I and -II. In addition the proinflammatory cytokines IL-1 ␤ and TNF-␣ produced increases in

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“…In Crohn's disease, expression of insulin-like growth factor-I (IGF-I) is increased in all layers of the intestine including the muscularis propria (37). Similar events occur in animal models of chronic intestinal inflammation: TNBS-induced and dextran sulfateinduced colitis (28,33) and peptidoglycan-polysaccharideinduced ileocolitis (38). IGF-I is an endogenous growth factor that plays a central role in the growth and development of visceral and vascular smooth muscle.…”

mentioning

confidence: 97%

Endogenous IGF-I and α_vβ₃ integrin ligands regulate increased smooth muscle growth in TNBS-induced colitis

Hazelgrove

Flynn²,

Qiao³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Hazelgrove KB, Flynn RS, Qiao LY, Grider JR, Kuemmerle JF. Endogenous IGF-I and ␣v␤3 integrin ligands regulate increased smooth muscle growth in TNBS-induced colitis. Am J Physiol Gastrointest Liver Physiol 296: G1230 -G1237, 2009. First published April 9, 2009 doi:10.1152/ajpgi.90508.2008.-Endogenous insulinlike 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 ␣v␤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 ␣ v␤3 integrin expression was not altered by TNBSinduced colitis, vitronectin and fibronectin levels were increased by 80 Ϯ 10% and 90 Ϯ 15%, above control levels, respectively. Basal IGF-I receptor phosphorylation in inflamed muscle from TNBStreated rats was increased by 86 Ϯ 8% over vehicle-treated controls. Basal ERK1/2, p70S6 kinase, and GSK-3␤ phosphorylation in muscle cells of TNBS-treated rats were also increased by 140 -180%. TNBS treatment increased basal muscle cell proliferation by 130 Ϯ 15% and decreased apoptosis by 20 Ϯ 2% compared with that in vehicletreated controls. The changes in proliferation and apoptosis were reversed by an IGF-I receptor tyrosine kinase inhibitor or an ␣v␤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 ␣ v␤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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Insulinlike growth factor I and interleukin 1β messenger RNA in a rat model of granulomatous enterocolitis and hepatitis

Cited by 86 publications

References 34 publications

Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Regulation of proliferation of human colonic subepithelial myofibroblasts by mediators important in intestinal inflammation.

Endogenous IGF-I and α_vβ₃ integrin ligands regulate increased smooth muscle growth in TNBS-induced colitis

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Insulinlike growth factor I and interleukin 1β messenger RNA in a rat model of granulomatous enterocolitis and hepatitis

Cited by 86 publications

References 34 publications

Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Altered liver gene expression in CCl4-cirrhotic rats is partially normalized by insulin-like growth factor-I

Regulation of proliferation of human colonic subepithelial myofibroblasts by mediators important in intestinal inflammation.

Endogenous IGF-I and αvβ3 integrin ligands regulate increased smooth muscle growth in TNBS-induced colitis

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Endogenous IGF-I and α_vβ₃ integrin ligands regulate increased smooth muscle growth in TNBS-induced colitis