Gene expression of the insulin-like growth factor system during mouse kidney development

Lindenbergh-Kortleve, Dicky J.; Rosato, Roberto R.; Neck, Johan W. van; Nauta, Jeroen; Kleffens, Marjolein van; Groffen, Cora; Zwarthoff, Ellen C.; Drop, Stenvert L. S.

doi:10.1016/s0303-7207(97)00123-8

Cited by 56 publications

(55 citation statements)

References 42 publications

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“…We show that, at early stages of nephrogenesis, IGF-II/M6PR is localized in the nephrogenic zone, especially in undifferentiated mesenchymal cells. IGF-II mRNA is abundant in developing kidney in mice and humans and is mainly expressed in the mesenchymal cells (36,37). The colocalization of the receptor with the growth factor and the increase in the IGF-II/M6PR protein we observed in the kidneys of fetuses from diabetic mothers may thus reduce the bioavailability of IGF-II in this organ.…”

Section: Diabetes Vol 50 May 2001mentioning

confidence: 65%

Altered Nephrogenesis Due to Maternal Diabetes Is Associated With Increased Expression of IGF-II/Mannose-6-Phosphate Receptor in the Fetal Kidney

et al. 2001

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We have recently demonstrated that the exposure to hyperglycemia in utero impairs nephrogenesis in rat fetuses (Amri K et al., Diabetes 48:2240 -2245, 1999). Diabetic pregnancy is commonly associated with alterations in the IGF system in fetal tissues. It has also been shown that both IGF-I and IGF-II are produced within developing metanephros and promote renal organogenesis. Therefore, we investigated the effect of maternal diabetes on IGFs and their receptors in developing fetal rat kidney. Diabetes was induced in pregnant rats by a single injection of streptozotocin on day 0 of gestation. We measured the amounts of IGF and their receptors, both proteins and mRNAs, in the metanephroi of fetuses issued from diabetic subjects and in age-matched fetuses from control subjects (14 -20 days of gestation). IGF-II was produced throughout fetal nephrogenesis, whereas IGF-I protein was not detected, suggesting a critical role of IGF-II in kidney development. Fetal exposure to maternal diabetes caused no change in IGF production in the early stages of nephrogenesis. Similarly, the amounts of IGF-I receptor and insulin receptor were not altered. By contrast, there was an increase in production of IGF-II/mannose-6-phosphate receptor throughout nephrogenesis. Because this receptor plays an essential role in regulating the action of IGF-II, the altered nephrogenesis in fetuses exposed to maternal diabetes may be linked to a decrease in IGF-II bioavailability.

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Section: Diabetes Vol 50 May 2001mentioning

confidence: 65%

Altered Nephrogenesis Due to Maternal Diabetes Is Associated With Increased Expression of IGF-II/Mannose-6-Phosphate Receptor in the Fetal Kidney

et al. 2001

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“…This increase in renal IGFBP-1 mRNA expression in potassium-deficient rats was not affected by IGF-I infusion (van Neck et al 1997).…”

Section: Introductionmentioning

confidence: 71%

“…In various conditions characterized by renal growth, renal IGFBP-1 levels have been reported to be elevated (e.g. diabetes mellitus, hypokalemia) (Flyvbjerg 1993, Hsu et al 1997, van Neck et al 1997.…”

Section: Introductionmentioning

confidence: 99%

The role of the IGF axis in IGFBP-1 and IGF-I induced renal enlargement in Snell dwarf mice

Kleffens

Lindenbergh-Kortleve

Koster³

et al. 2001

Journal of Endocrinology

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Insulin-like growth factor (IGF) binding protein-1 (IGFBP-1) is generally believed to inhibit IGF action in the circulation. In contrast, IGFBP-1 has been reported to interact with cell surfaces and enhance IGF-I action locally in some tissues. Renal IGFBP-1 levels are found elevated in various conditions characterized by renal growth (e.g. diabetes mellitus, hypokalemia).To test whether IGFBP-1 is a renotropic factor, IGFBP-1 was administered alone or in combination with IGF-I to Snell dwarf mice, an in vivo model without compensatory feedback effects on growth hormone (GH) secretion. In three control groups of Snell dwarf mice, placebo, GH or IGF-I was administered. Compared with placebo, kidney weight increased in all treated groups, however, with different effects on kidney morphology. Administration of IGF-I, alone or in combination with IGFBP-1, tended to increase glomerular volume, while no changes were seen in the other groups. Administration of IGFBP-1 or IGFBP-1+IGF-I both caused dilatation of the thin limbs of Henle's loop, while GH or IGF-I administration had no visible effect. Furthermore, IGF-I administration resulted in an increased mean number of nuclei per cortical area and renal weight, whereas GH, IGF-I+IGFBP-1 or IGFBP-1 caused a decreased renal nuclei number.In situ hybridization and immunohistochemistry showed specific changes of the renal IGF system expression patterns in the different groups. Particularly, IGFBP-1 administration resulted in extensive changes in the mRNA expression of the renal IGF system, whereas the other administration regimen resulted in less prominent modifications. In contrast, administration of IGFBP-1 and IGFBP-1+IGF-I resulted in identical changes in the protein expression of the renal IGF system.Our results indicate that IGFBP-1, alone or in combination with IGF-I, demonstrated effects on the renal tubular system that differ from the effects of IGF-I.

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“…The non-competitive quantitative RT-PCR was performed as previously described (33) following the method originally reported by Pane et al (34). An absolute amount of mRNA molecules is calculated by interpolating the generated amount of PCR products from sample RNA into a titration curve obtained by amplifying a known number of synthetic RNA molecules containing the same sequence as the RNA to be quantitated.…”

Section: Quantitative Rt-pcrmentioning

confidence: 99%

“…The synthetic mRNA used as standard was obtained as previously reported (33). Briefly, cDNA fragments of the desired sequences were amplified by performing PCR on the available cDNAs of the mouse IGF system (35).…”

Section: Quantitative Rt-pcrmentioning

confidence: 99%

Effect of chronic thyroxine treatment on IGF-I, IGF-II and IGF-binding protein expression in mammary gland and liver during pregnancy and early lactation in rats

Rosato

Lindenbergh-Kortleve

Neck

et al. 2002

European Journal of Endocrinology

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Objective: Hyperthyroidism in rats produces organ hypertrophy and increases in circulating IGF-I and IGF-binding protein (IGFBP)-3. Chronic treatment with thyroxine (T 4 ) during pregnancy advances parturition, blocks lactation and changes several hormone receptors in mammary gland and liver. Since IGFs are implicated in mammary and liver growth and in differentiation, we studied the effects of hyperthyroidism, induced by daily injections of T 4 (0.25 mg/kg). Design and Methods: Using quantitative RT-PCR and in situ hybridization, the gene expression of IGF-I, IGF-II and the IGFBPs was determined in mammary gland and liver of rats at estrus and days 7, 14 and 21 of pregnancy (G7, G14, G21), day 1 postpartum (L1) and 3 days after removing the litter (L4). Circulating levels of IGF-I, tri-iodothyronine (T 3 ), PRL and GH were measured. Results: T 4 treatment (HT) increased circulating T 3 save on G21, did not change serum IGF-I, increased PRL on G21 and decreased GH on L1. PRL decreased on L1 because of the absence of lactation. Hepatic IGF-I mRNA was low during pregnancy and increased on L4. HT advanced this increase to L1. In controls, liver IGFBP-3 mRNA levels decreased from G14 to G21, whereas IGFBP-4 showed an inverse pattern. HT lowered IGFBP-3 mRNA and increased IGFBP-4. Increases in mammary concentrations of IGF-I, IGFBP-3 and IGFBP-4 mRNAs were seen on G21. HT delayed these peaks to L1. Mammary IGF-II and IGFBP-2 mRNA levels were high on G7 and G14, and fell afterwards, with HT having no effects. IGFBP-5 mRNA decreased during pregnancy and increased on L1. HT increased IGFBP-5 levels in early pregnancy and on L1. IGF-I mRNA localized to connective and epithelial mammary tissue, while IGFBP-2 and IGFBP-5 mRNA was only in epithelial cells. Conclusion: These results imply a role for IGF-I, IGFBP-3 and IGFBP-4 in terminal mammary development, while IGF-II and IGFBP-2 may be implicated in early growth. IGFBP-5 has been implicated in mammary apoptosis, and the HT-induced increase may play a role in the premature mammary involution of the HT rats.

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Gene expression of the insulin-like growth factor system during mouse kidney development

Cited by 56 publications

References 42 publications

Altered Nephrogenesis Due to Maternal Diabetes Is Associated With Increased Expression of IGF-II/Mannose-6-Phosphate Receptor in the Fetal Kidney

Altered Nephrogenesis Due to Maternal Diabetes Is Associated With Increased Expression of IGF-II/Mannose-6-Phosphate Receptor in the Fetal Kidney

The role of the IGF axis in IGFBP-1 and IGF-I induced renal enlargement in Snell dwarf mice

Effect of chronic thyroxine treatment on IGF-I, IGF-II and IGF-binding protein expression in mammary gland and liver during pregnancy and early lactation in rats

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