The effect of epidermal growth factor and IGF-I infusion on hepatic and renal expression of the IGF-system in adult female rats

Neck, Johan W. van; Berghout, E. M.; Vinter‐Jensen, Lars; Groffen, Cora; Cingel, Vesna; Dits, Natasja F.; Drop, Stenvert L. S.; Flyvbjerg, Allan

doi:10.1677/joe.0.1650115

Cited by 12 publications

(11 citation statements)

References 27 publications

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“…As discussed, downregulation of IGFBPs can occur at the transcriptional level or at the post-translational level (Vinter-Jensen et al 1996, Edmondson et al 1999, van Neck et al 2000, Ozawa et al 2004. Our data demonstrating reduced IGFBP-3 and -4 mRNA levels support a transcriptional regulatory mechanism.…”

Section: Discussionsupporting

confidence: 70%

“…Furthermore, administration of EGF to neonatal rats resulted in reduced body weight, decreased circulating IGF-I, and increased serum IGFBP-1 levels (Murray et al 1993, van Neck et al 2000. However, EGF administration to adult female rats did not result in a reduction of growth (van Neck et al 2000). Our data demonstrates that a second EGFR ligand, HB-EGF, retards growth early in development through an IGF-related pathway.…”

Section: Discussionmentioning

confidence: 67%

“…A similar transgenic mouse model overexpressing EGF exhibited a 50% reduction in body mass at birth, which then increased to 80% of normal at approximately 3 weeks of age (Chan and Wong 2000). Furthermore, administration of EGF to neonatal rats resulted in reduced body weight, decreased circulating IGF-I, and increased serum IGFBP-1 levels (Murray et al 1993, van Neck et al 2000. However, EGF administration to adult female rats did not result in a reduction of growth (van Neck et al 2000).…”

Section: Discussionmentioning

confidence: 99%

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Heparin-binding EGF-like growth factor (HB-EGF) overexpression in transgenic mice downregulates insulin-like growth factor binding protein (IGFBP)-3 and -4 mRNA

et al. 2005

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An in vivo approach was taken to assess the biological significance of heparin-binding EGF-like growth factor (HB-EGF) using transgenic mice. Transgenic mice were generated using the pIRES-EGFP vector expressing a bicistronic mRNA containing both human HB-EGF (hHB-EGF) and enhanced green fluorescent protein (EGFP) coding sequences under the regulation of the cytomegalovirus immediate-early (CMV-IE) promoter. As a marker for transgene expression, EGFP fluorescence in 5 microm tissue sections was evaluated. To confirm HB-EGF expression in EGFP-containing tissues, HB-EGF mRNA was analyzed by RT-PCR and Northern blot analysis. Protein levels of HB-EGF and insulin-like growth factor binding protein-3 (IGFBP-3), a molecule that stabilizes IGFs, which in turn helps to promote growth, were analyzed by Western blot. Also, the weights of transgenic mice were compared with the weights of wild type non-transgenic littermates over a 10-week period. EGFP fluorescence, RT-PCR and Northern analysis of a variety of tissues from hHB-EGF transgenic mice indicate recombinant EGFP/hHB-EGF mRNA expression in kidney, liver, lung and stomach. Western blot analysis confirmed that HB-EGF protein levels were greater in these tissues from hHB-EGF transgenic mice compared to wild type non-transgenic littermates. IGFBP-3 protein was absent in serum of transgenic mice prior to the onset of puberty, but indistinguishable from wild type non-transgenic mice after puberty. Furthermore, IGFBP-3 and IGFBP-4 mRNA were downregulated in the kidney, but not liver or lung of the transgenic mice. In accordance with reduced IGFBP-3 and -4 levels, hHB-EGF transgenic mice exhibited a 20% decrease in weight prior to 6 weeks of age compared to wild type non-transgenic littermates. Our laboratory has generated a biologically functional transgenic mouse model exhibiting increased expression of hHB-EGF in kidney, liver, lung and stomach. Overexpression of hHB-EGF affected the growth rate of these transgenic mice possibly through a pathway involving IGFBP-3 and IGFBP-4.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

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Heparin-binding EGF-like growth factor (HB-EGF) overexpression in transgenic mice downregulates insulin-like growth factor binding protein (IGFBP)-3 and -4 mRNA

et al. 2005

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“…It is known that IGF-I is a stimulant of IGFBP synthesis in rat liver [26]. Our result showed the increase of hepatic IGF-I and IGF-II expressions in HP-UN and BCAA-UN, so that the elevated IGFBPs in fetal liver might be the result of an increased IGF expression.…”

Section: Discussionsupporting

confidence: 49%

Isocaloric high-protein diet as well as branched-chain amino acids supplemented diet partially alleviates adverse consequences of maternal undernutrition on fetal growth

Mogami

Yura

Itoh

et al. 2009

Growth Hormone & IGF Research

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Maternal undernutrition causes fetal growth restriction. Protein is a vital dietary nutrient for fetal growth, and branched-chain amino acids (BCAA) are noted to have anabolic actions. In this study, we investigated the effects of maternal high-protein diet or BCAA-supplemented diet upon fetal growth under the condition of maternal calorie restriction. Pregnant mice were calorie-restricted (undernutrition: UN), using either a standard diet (S-UN group), high-protein diet (HP-UN group), or BCAA-supplemented diet (BCAA-UN group) to 70% of the control; dams fed ad libitum with a standard diet (S-NN group) from 10.5days post coitum (dpc) to 18.5dpc. The fetal weights of UN groups were significantly decreased compared to that of S-NN. However, the fetal weights of HP-UN and BCAA-UN were significantly higher by 5% and 4%, respectively, than those of S-UN, concomitant with augmentation of the gene and protein expressions of IGF-I and IGF-II in fetal liver. A high-protein diet as well as BCAA-supplemented diet partially improved fetal growth restriction caused by maternal calorie-restriction, suggesting a pivotal role of them in the amelioration of fetal growth restriction.

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“…Scharf et al (1996) reported that IGF-I is a potent stimulator for the synthesis of IGFBP-3 and ALS, in co-cultures of Kupffer cells and hepatocytes in adult rats, and that GH did not exert direct effects on IGFBP-3 synthesis, but stimulated the expression of ALS. In adult female rats, serum IGFBP-3 as well as hepatic IGFBP-3 mRNA levels increased after IGF-I treatment (van Neck et al 2000). In contrast, IGF-I mRNA levels and IGFBP-3 mRNA in the liver were reduced in hypophysectomized rats, and GH treatment increased both of them (Domene et al 1993).…”

Section: Discussionmentioning

confidence: 91%

Arthritis-induced increase in serum levels of IGF-binding protein-3 in rats is secondary to the decrease in its proteolytic activity

Cáceres¹,

Holly²,

Priego³

et al. 2002

Journal of Endocrinology

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Adjuvant-induced arthritis is a chronic inflammatory illness that induces a catabolic state, with a decrease in pituitary GH and hepatic IGF-I synthesis. We have previously observed an increase in serum IGF-binding protein-3 (IGFBP-3) in arthritic rats, and found that GH administration prevents the increase in circulating IGFBP-3 in arthritic rats. The aim of this work was therefore to study IGFBP-3 synthesis in the liver as well as its proteolysis in serum as the two possible causes of the increased circulating IGFBP-3 in arthritic rats. The effect of recombinant human GH (rhGH) administration was also analysed. Adult male Wistar rats were injected with complete Freund's adjuvant or vehicle, and 14 days later they were injected s.c. daily until day 22 after adjuvant injection with rhGH (3 IU/kg) or saline. Three hours after the last GH injection, all rats were killed by decapitation. Arthritis increased serum IGFBP-3 levels (P<0·01). The increase in serum IGFBP-3 levels in arthritic rats seems to be due to decreased proteolysis (P<0·01) rather than to an increased synthesis, since liver IGFBP-3 mRNA content was not modified by arthritis. GH administration to control rats resulted in an increase in both hepatic IGFBP-3 mRNA content and in serum IGFBP-3 levels in spite of the increase in IGFBP-3 proteolysis in serum. In arthritic rats, GH treatment did not modify liver IGFBP-3 synthesis, but it increased serum proteolysis of IGFBP-3, leading to a serum concentration of IGFBP-3 similar to that of control rats. Furthermore, there was a negative correlation between circulating IGFBP-3 and its proteolytic activity in the serum of adjuvant-induced arthritic rats. These data suggest that in chronic arthritis the increase in IGFBP-3 serum concentration is secondary to a decrease in proteolytic activity, rather than to an increase in hepatic IGFBP-3 gene expression.

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The effect of epidermal growth factor and IGF-I infusion on hepatic and renal expression of the IGF-system in adult female rats

Cited by 12 publications

References 27 publications

Heparin-binding EGF-like growth factor (HB-EGF) overexpression in transgenic mice downregulates insulin-like growth factor binding protein (IGFBP)-3 and -4 mRNA

Heparin-binding EGF-like growth factor (HB-EGF) overexpression in transgenic mice downregulates insulin-like growth factor binding protein (IGFBP)-3 and -4 mRNA

Isocaloric high-protein diet as well as branched-chain amino acids supplemented diet partially alleviates adverse consequences of maternal undernutrition on fetal growth

Arthritis-induced increase in serum levels of IGF-binding protein-3 in rats is secondary to the decrease in its proteolytic activity

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