Gene expression patterns of insulin-like growth factor 1, insulin-like growth factor 2 and insulin-like growth factor binding protein 3 in human placenta from pregnancies with intrauterine growth restriction

Börzsönyi, Balázs; Demendi, Csaba; Nagy, Zsolt B.; Tóth, Katalin; Csanád, Mónika; Pajor, Attila; Rig, János; Joó, József Gábor

doi:10.1515/jpm.2011.090

Cited by 24 publications

(12 citation statements)

References 35 publications

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“…In male placentae, microvessel dilatation in the face of maternal hypertension preserves placental perfusion, size, and fetal growth rate [ 166 , 167 ]. In response to maternal nutrient deprivation, IGF2 synthesis and secretion become elevated in male placentae and male fetal growth is again preserved compared to female fetal growth [ 168 ]. The absence of these adaptations in female placentae is associated with reduction and retardations in in utero growth but increased survival.…”

Section: Developmental Origins Of Sex Differencesmentioning

confidence: 99%

An integrative view on sex differences in brain tumors

Sun

Plutynski

Ward

et al. 2015

Cell. Mol. Life Sci.

169

120

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Sex differences in human health and disease can range from undetectable to profound. Differences in brain tumor rates and outcome are evident in males and females throughout the world and regardless of age. These observations indicate that fundamental aspects of sex determination can impact the biology of brain tumors. It is likely that optimal personalized approaches to the treatment of male and female brain tumor patients will require recognizing and understanding the ways in which the biology of their tumors can differ. It is our view that sex-specific approaches to brain tumor screening and care will be enhanced by rigorously documenting differences in brain tumor rates and outcomes in males and females, and understanding the developmental and evolutionary origins of sex differences. Here we offer such an integrative perspective on brain tumors. It is our intent to encourage the consideration of sex differences in clinical and basic scientific investigations.

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Section: Developmental Origins Of Sex Differencesmentioning

confidence: 99%

An integrative view on sex differences in brain tumors

Sun

Plutynski

Ward

et al. 2015

Cell. Mol. Life Sci.

169

120

View full text Add to dashboard Cite

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“…IGF1 gene ablation has been shown to reduce fetal weight while IGF1 administration has been shown to increase fetal weight [ 4 ]. The main role of IGF2 appears to be mediated through its effects on cellular growth and tissue-specific cell proliferation [ 5 ]. IGF2 overexpression in mice causes placental and fetal overgrowth, whereas IGF2 gene deletion reduces placental and fetal weight [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Insulin-like growth factor axis in pregnancies affected by fetal growth disorders

et al. 2016

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BackgroundInsulin-like growth factors 1 and 2 (IGF1 and IGF2) and their binding proteins (IGFBPs) are expressed in the placenta and known to regulate fetal growth. DNA methylation is an epigenetic mechanism which involves addition of methyl group to a cytosine base in the DNA forming a methylated cytosine-phosphate-guanine (CpG) dinucleotide which is known to silence gene expression. This silences gene expression, potentially altering the expression of IGFs and their binding proteins. This study investigates the relationship between DNA methylation of components of the IGF axis in the placenta and disorders in fetal growth. Placental samples were obtained from cord insertions immediately after delivery from appropriate, small (defined as birthweight <10th percentile for the gestation [SGA]) and macrosomic (defined as birthweight > the 90th percentile for the gestation [LGA]) neonates. Placental DNA methylation, mRNA expression and protein levels of components of the IGF axis were determined by pyrosequencing, rtPCR and Western blotting.ResultsIn the placenta from small for gestational age (SGA) neonates (n = 16), mRNA and protein levels of IGF1 were lower and of IGFBPs (1, 2, 3, 4 and 7) were higher (p < 0.05) compared to appropriately grown neonates (n = 37). In contrast, in the placenta from large for gestational age (LGA) neonates (n = 20), mRNA and protein levels of IGF1 was not different and those of IGFBPs (1, 2, 3 and 4) were lower (p < 0.05) compared to appropriately grown neonates. Compared to appropriately grown neonates, CpG methylation of the promoter regions of IGF1 was higher in SGA neonates. The CpG methylation of the promoter regions of IGFBP1, IGFBP2, IGFBP3, IGFBP4 and IGFBP7 was lower in the placenta from SGA neonates as compared to appropriately grown neonates, but was unchanged in the placenta from LGA neonates.ConclusionsOur results suggest that changes in CpG methylation contribute to the changes in gene expression of components of the IGF axis in fetal growth disorders. Differential methylation of the IGF1 gene and its binding proteins is likely to play a role in the pathogenesis of SGA neonates.

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“…In placentas from males from preterm deliveries, there is an overexpression of both IGF-2 and IGFBP-3 genes [19]. Further, in placentas from pregnancies with IUGR, IGF-2 is also overexpressed reflecting its physiological role in optimizing energy distribution in a low-energy environment [20]. Cord serum concentrations of IGF-2 have been shown to have a significant positive effect on both birth length and weight and cord serum IGFBP-2 concentrations have been shown to correlate positively with weight gain during infancy [21,22].…”

Section: Introductionmentioning

confidence: 99%

Maternal nutritional history modulates the hepatic IGF–IGFBP axis in adult male rat offspring

et al. 2013

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Alterations in early life nutrition lead to an increased risk of obesity and metabolic syndrome in offspring. We have shown that both relative maternal undernutrition (UN) and maternal obesity result in metabolic derangements in offspring, independent of the postnatal dietary environment. Since insulin-like growth factor binding protein 2 (IGFBP2) has been shown to be independently associated with obesity and diabetes risk, we examined the IGF-IGFBP axis in male rat offspring following either maternal UN or maternal obesity to explain possible common pathways in the development of metabolic disorders. Wistar rats were time-mated and fed either a control diet (CONT), 50 % of CONT (UN) or a high-fat (HF) diet throughout pregnancy. Male offspring were weaned onto a standard chow diet and blood and tissues were collected at postnatal day 160. Plasma and hepatic tissue samples were analysed for key players in the IGF-IGFBP system. Both maternal UN and HF resulted in increased fat mass, hyperinsulinemia, hyperleptinemia and altered blood lipid profiles in offspring compared to CONT. Circulating IGF-1 and IGFBP3 levels and hepatic mRNA expression of IGFBP1 and IGFBP2 were significantly decreased in UN and HF offspring compared to CONT. DNA methylation of the IGFBP2 promotor region was similar between maternal dietary groups. Although chaperone gene heat-shock protein 90 and hepatic IGFBP1 were significantly correlated in CONT offspring this effect was absent in both UN and HF offspring. In conclusion, this study is one of the first to directly compare two experimental models of developmental programming representing both ends of the maternal dietary spectrum. Our data suggest that two disparate nutritional models that elicit similar adverse metabolic phenotypes in offspring are characterised by common alterations in the IGF-IGFBP pathway.

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Gene expression patterns of insulin-like growth factor 1, insulin-like growth factor 2 and insulin-like growth factor binding protein 3 in human placenta from pregnancies with intrauterine growth restriction

Cited by 24 publications

References 35 publications

An integrative view on sex differences in brain tumors

An integrative view on sex differences in brain tumors

Insulin-like growth factor axis in pregnancies affected by fetal growth disorders

Maternal nutritional history modulates the hepatic IGF–IGFBP axis in adult male rat offspring

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