Morphometric evidence that villous development and fetoplacental angiogenesis are compromised by intrauterine growth restriction but not by pre-eclampsia

Mayhew, Terry M.; Wijesekara, J.; Baker, Philip N.; Ong, Stephen

doi:10.1016/j.placenta.2004.04.011

Cited by 145 publications

(90 citation statements)

References 26 publications

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“…38 It is believed that pre-eclampsia and FGR share common components in their pathogenesis, although some disparate findings have been described. 7,39 Furthermore, it has been suggested that FGR in pre-eclampsia represents the response to a fetal signal stimulated by reduced placental nutrient availability that is inadequate to overcome the subsequent malnutrition stress. Conversely, FGR without pre-eclampsia occurs as a result of the absence of this signal.…”

Section: Discussionmentioning

confidence: 99%

Reduced placental prolyl hydroxylase 3 mRNA expression in pregnancies affected by fetal growth restriction

Gourvas

Sifakis

Dalpa

et al. 2010

BJOG

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Objective To investigate the role of the hypoxia-inducible factor (HIF) pathway in fetal growth restriction (FGR).Design A case-control study.Setting Research laboratory and gynaecology clinic.Sample Twenty placentas from normal pregnancies and 20 from FGR pregnancies.Methods RNA extraction, cDNA synthesis, quantitative real-time polymerase chain reaction (qRT-PCR) assay, statistical analysis.Main outcome measures mRNA expression of HIF-1a, HIF-2a and HIF-b (ARNT), along with prolyl hydroxylase domain 3 (PHD3), which leads to proteasomal degradation of HIF-a subunits.Results No statistically significant differences in the transcription levels of ARNT and HIF-2a were found between FGR and normal placentas. By contrast, PHD3 and HIF-1a mRNA were downregulated in FGR placentas. PHD3 mRNA expression was associated with gestational age at delivery (P = 0.008), birthweight centile (P = 0.029) and abnormal umbilical artery (UA) Doppler measurements (P = 0.034).Conclusions As PHD3 regulates the HIF-mediated hypoxic response in FGR, we deduce that fetal adaptation to hypoxia ranges from impaired to adequate, as observed by the gradient of PHD3 downregulation in relation to the severity of FGR.

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Section: Discussionmentioning

confidence: 99%

Reduced placental prolyl hydroxylase 3 mRNA expression in pregnancies affected by fetal growth restriction

Gourvas

Sifakis

Dalpa

et al. 2010

BJOG

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“…In preeclamptic women, uteroplacental hypoperfusion is frequently observed, leading to growth restriction of the fetus [14]. Placental dysfunction is also suggested in non-preeclamptic women with SGA infants [22,23]. However, it has been controversial whether placental leptin production has any correlation with deterioration in fetal growth.…”

Section: Discussionmentioning

confidence: 99%

The Relationship between Maternal Plasma Leptin Levels and Fetal Growth Restriction

et al. 2007

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Abstract. Leptin is a satiety hormone secreted from the adipose tissue and human placenta. We previously demonstrated that severe preeclampsia up-regulated leptin mRNA expression in the placenta and elevated maternal plasma leptin concentrations. Preeclampsia is frequently related to generation of small for gestational age (SGA) infant especially in cases with severe preeclampsia. However, it is still controversial whether the increase in maternal plasma leptin levels is associated with fetal growth restriction without complication of preeclampsia. Therefore, the aim of the present study was to explore the relationship between maternal plasma leptin levels and fetal growth in non-preeclamptic (n = 98) and preeclamptic (n = 40) women. In non-preeclamptic pregnant women, plasma leptin levels in SGA group (n = 11) were significantly higher than those in appropriate for gestational age (AGA) group (n = 87, P<0.05). In pregnant women with preeclampsia, likewise, plasma leptin levels in SGA group (n = 15) were significantly higher than those in AGA group (n = 25, P<0.05). In multiple linear regression analysis, maternal BMI, mean arterial blood pressure and ∆SD of neonatal body weight were significant factors for determining maternal plasma leptin levels in all population studied. Maternal BMI and ∆SD of neonatal body weight showed positive correlation with maternal plasma leptin levels when analysis was performed in non-preeclamptic subjects alone. In conclusion, maternal plasma leptin levels reflect, at least partly, deterioration in fetal growth.

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“…Therefore, an early detection of intrauterine growth retardation (IUGR) will be beneficial to obstetric and neonatal care [8]. Studies have shown that diminished placental size precedes fetal growth retardation as IUGR is associated with impoverished villous development and fetoplacental angiogenesis [9,10].The present study was undertaken in our institution to study the correlation of placental thickness, measured at the level of the umbilical cord insertion, with the ultrasonographic gestational age in normal and IUGR pregnancies in the late second and third trimester ( Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

Placental Thickness: Its Correlation with Ultrasonographic Gestational Age in Normal and Intrauterine Growth-Retarded Pregnancies in the Late Second and Third Trimester

Mathai¹,

Singla²,

Nittala

et al. 2013

J Obstet Gynecol India

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Morphometric evidence that villous development and fetoplacental angiogenesis are compromised by intrauterine growth restriction but not by pre-eclampsia

Cited by 145 publications

References 26 publications

Reduced placental prolyl hydroxylase 3 mRNA expression in pregnancies affected by fetal growth restriction

Reduced placental prolyl hydroxylase 3 mRNA expression in pregnancies affected by fetal growth restriction

The Relationship between Maternal Plasma Leptin Levels and Fetal Growth Restriction

Placental Thickness: Its Correlation with Ultrasonographic Gestational Age in Normal and Intrauterine Growth-Retarded Pregnancies in the Late Second and Third Trimester

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