Localization of mRNAs for insulin-like growth factor binding proteins 1 to 6 in rat kidney

Price, Glynis; Berka, Jennifer L.; Edmondson, Stephanie R.; Werther, George A.; Bach, Leon A.

doi:10.1038/ki.1995.308

Cited by 33 publications

(26 citation statements)

References 21 publications

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“…A complicating factor in matching our findings with the literature is that descriptions of changed IGF system expression patterns in renal disease models are scarce and, if existing, are often derived from rat studies where, compared with mice, differences in IGF system expression are observed, especially regarding IGFBP-1 expression (Chin et al 1992, Price et al 1995, Rabkin et al 1995, Lindenbergh-Kortleve et al 1997.…”

Section: Effects On Renal Expression Of Igf System Componentsmentioning

confidence: 66%

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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Section: Effects On Renal Expression Of Igf System Componentsmentioning

confidence: 66%

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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“…The remaining 20% of the IGFs are associated with IGFBP-1, -2, or -4 in a smaller complex, which can diffuse into the intravascular space, target IGFs to tissues, and modulate their bioavailability by inhibiting or potentiating their actions (21). In the kidney, IGFBPs are heterogeneously distributed to support their modulatory role in IGF actions (11,22,23). The overexpression of hIGFBP-1 in our transgenic mice (13.7 Ϯ 1.4 ng/mL and 3.0 Ϯ 0.4 ng/mL in homozygous and heterozygous mice, respectively) remained stable with age (14).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Human Insulin-Like Growth Factor Binding Protein-1 in the Mouse Leads to Nephron Deficit

et al. 2001

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“…14 However IGFBP-1 mRNA is found in a small percentage of kidney cells, perhaps reflecting the lesser DNaseI hypersensitivity. 58 Weak liver specific sites at Ϫ800 (HS2) and Ϫ2,300 (HS3) were also detected. All sites were confirmed in several animals and with different restriction enzymes and probes (data not shown).…”

Section: Tissue-specific Dnasei Hypersensitivity Sites Within the Igfmentioning

confidence: 99%

Liver-specific and proliferation-induced deoxyribonuclease I hypersensitive sites in the mouse insulin-like growth factor binding protein-1 gene

et al. 1999

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The insulin-like growth factor binding protein-1 (IGFBP-1) gene is highly expressed in fetal, perinatal, and regenerating liver. Up-regulation is transcriptionally mediated in regenerating liver and occurs in the first few minutes to hours after partial hepatectomy. In transgenic mice a 970-bp region from ؊776 to ؉151 of the IGFBP-1 promoter was sufficient for tissue-specific and induced expression of the gene in fetal and hepatectomized livers. However weak and/or poorly regulated expression in some transgenic lines suggested the existence of other regulatory regions. Here, genomic clones containing large regions 5Ј of the mouse IGFBP-1 gene sequence were isolated, subcloned, and sequenced. Deoxyribonuclease I (DNaseI) hypersensitivity analyses identified clusters of tissue-specific nucleasesensitive sites in the promoter region, ؊100 to ؊300, ؊2,300, ؊3,100, and ؊5,000 along with other weak sites. After partial hepatectomy, enhanced sensitivity and/or novel sites were detected in the ؊100/؊300, ؊5,000, and ؊3,100 regions, the promoter region remaining the most hypersensitive. A subset of these sites was present in fetal and perinatal livers. Novel tissue-specific sites that interacted with C/EBP and hepatic nuclear factor 3 (HNF3) transcription factors were identified in the ؊3,100 region. A hepatectomy-induced DNA binding complex containing the transcription factor USF1 was identified within the ؊100 to ؊300 region of the promoter. These results suggested that a complex array of tissue-specific and hepatic proliferationinduced transcription factors combine to regulate both the proximal promoter and more distal regulatory elements of the

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Localization of mRNAs for insulin-like growth factor binding proteins 1 to 6 in rat kidney

Cited by 33 publications

References 21 publications

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

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

Overexpression of Human Insulin-Like Growth Factor Binding Protein-1 in the Mouse Leads to Nephron Deficit

Liver-specific and proliferation-induced deoxyribonuclease I hypersensitive sites in the mouse insulin-like growth factor binding protein-1 gene

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