Insulin-like growth factor 2 and short-range stimulatory loops in control of human placental growth.

Ohlsson, Rolf; Holmgren, Lars; Glaser, Anna; Szpecht, A; Pfeifer-Ohlsson, Susan

doi:10.1002/j.1460-2075.1989.tb03606.x

Cited by 122 publications

(73 citation statements)

References 16 publications

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“…IGF-II is produced by the invasive extravil-lous trophoblast (EVT) in baboons and humans [39][40][41] and by decidua and trophoblast in guinea pigs [42]. In our study, both IGF-II mRNA and protein expression were detected in syncytiotrophoblast and cytotrophoblast with increased expression in placentae of the NR group.…”

Section: Changes In the Placental Igf Systemmentioning

confidence: 52%

The IGF Axis in Baboon Pregnancy: Placental and Systemic Responses to Feeding 70% Global Ad Libitum Diet

Li¹,

Levitz²,

Hubbard³

et al. 2007

Placenta

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Information on the influence of poor maternal nutrition on the regulation of responses to pregnancy, placental and fetal growth and development is critical to a better understanding of pregnancy physiology and pathophysiology. We determined normal changes and effects of controlled and monitored moderate nutrient restriction (NR) (global nutrient intake reduced to 70% of food consumed by mothers feeding ad libitum from 0.16 to 0.5 of gestation) in the baboon, on important hematological, biochemical, and hormonal indices of fetal growth and placental function. Serum IGF-I:IGFBP-3 ratio was lower in pregnant than control non-pregnant baboons feeding ad libitum. Serum concentrations of total and free IGF-I were decreased in NR mothers compared with controls (p < 0.05). The decrease in fetal IGF-I did not reach significance (p = 0.057). Serum IGF-I: IGFBP-3 ratio was decreased by NR in both mothers and fetuses. Maternal serum IGF-II was unchanged by NR. Placental IGF-I mRNA and protein abundance were similarly reduced whereas IGF-II mRNA increased in placental tissue of NR compared to control mothers. Systemic (maternal) and local (placental) IGFBP-1 and IGFBP-3 mRNA and protein abundance were unchanged by NR. Type 1 IGF receptor protein in the syncytiotrophoblast increased in NR. Type 2 IGF receptor protein was present in the stem villi core, and decreased after NR. We conclude that moderate NR in this important non-human primate model significantly disrupts the maternal and placental IGF-IGFBP axis and influences placental expression of this key system at the gene and protein level. Changes observed appear to be directed toward preserving placental growth.

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Section: Changes In the Placental Igf Systemmentioning

confidence: 52%

The IGF Axis in Baboon Pregnancy: Placental and Systemic Responses to Feeding 70% Global Ad Libitum Diet

Li¹,

Levitz²,

Hubbard³

et al. 2007

Placenta

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“…IGF-II acts as an important modulator of placental cell proliferation and maturation (36). A positive correlation has been demonstrated between cord blood IGF-II and placental weight (37).…”

Section: Intrauterine Growthmentioning

confidence: 98%

Genetic disorders in the GH–IGF-I axis in mouse and man

Walenkamp

Wit²

2007

eur j endocrinol

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Animal knockout experiments have offered the opportunity to study genes that play a role in growth and development. In the last few years, reports of patients with genetic defects in GH-IGF-I axis have greatly increased our knowledge of genetically determined causes of short stature. We will present the animal data and human reports of genetic disorders in the GH-IGF-I axis in order to describe the role of the GH-IGF-I axis in intrauterine and postnatal growth. In addition, the effects of the GH-IGF-I axis on the development and function of different organ systems such as brain, inner ear, eye, skeleton, glucose homeostasis, gonadal function, and immune system will be discussed. The number of patients with genetic defects in the GH-IGF-I axis is small, and a systematic diagnostic approach and selective genetic analysis in a patient with short stature are essential to identify more patients. Finally, the implications of a genetic defect in the GH-IGF-I axis for the patient and the therapeutic options will be discussed.European Journal of Endocrinology 157 S15-S26

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“…Preparation of embryo sections, generation of the probes, and in situ hybridization were performed as described (Ohlsson et al 1989). The riboprobe was produced by using a plasmid clone containing a 680-bp HinfI-PstI human cDNA insert.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Parental imprinting: potentially active chromatin of the repressed maternal allele of the mouse insulin-like growth factor II (Igf2) gene.

Sasaki¹,

Jones²,

Chaillet³

et al. 1992

Genes Dev.

267

153

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The mouse insulin-like growth factor II (Igf2) gene, which is located on distal chromosome 7 (Chr7), has been shown previously to undergo tissue-specific parental imprinting. This imprinting results in expression of Igf2 from the paternally inherited chromosome and repression of the maternally inherited allele in most tissues of the developing embryo. We are using embryos with the maternal duplication and paternal deficiency of distal Chr7 to characterize the mechanism that underlies repression of the maternal allele. We show that the chromatin of the 5' region of the repressed Igf2 allele is potentially active for transcription rather than heterochromatic. In particular, a CpG island that comprises one of the two strong promoters is unmethylated at both parental alleles, and DNase I hypersensitive sites in and around the strong promoters are consistently present on both parental chromosomes. In agreement with the chromatin state, primary transcripts from the maternal Igf2 allele have been detected at low but significant levels. These findings differ from observations in other instances of imprinting, namely, X-chromosome inactivation and transgene imprinting in mice. Although no parent-specific differences were detected in either DNA methylation or sensitivity to nucleases at these promoters, we have observed parental methylation differences in a region several kilobases upstream of the first exon. The differential activity of the parental Igf2 alleles could be achieved through epigenetic modifications situated outside the promoters or by subtle and yet unidentified modifications at the promoters.

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Insulin-like growth factor 2 and short-range stimulatory loops in control of human placental growth.

Cited by 122 publications

References 16 publications

The IGF Axis in Baboon Pregnancy: Placental and Systemic Responses to Feeding 70% Global Ad Libitum Diet

The IGF Axis in Baboon Pregnancy: Placental and Systemic Responses to Feeding 70% Global Ad Libitum Diet

Genetic disorders in the GH–IGF-I axis in mouse and man

Parental imprinting: potentially active chromatin of the repressed maternal allele of the mouse insulin-like growth factor II (Igf2) gene.

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