Placental-fetal Interrelationship in IUGR Fetuses—A Review

Pardi, Giorgio; Marconi, Anna Maria; Cetin, Irene

doi:10.1053/plac.2002.0802

Cited by 250 publications

(124 citation statements)

References 25 publications

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“…From E9.5 onward, the major nutrient transport is provided by the function of the placenta. Placental defects that manifest in inappropriate vascularization, patterning, dilation, or perfusion result in impaired development or embryonic lethality (Pardi et al, 2002). Several gene mutations display placenta phenotypes that are comparable to our Cdh1 HA/HA mutant mice.…”

Section: Discussionsupporting

confidence: 60%

A Cdh1^HA knock‐in allele rescues the Cdh1^−/− phenotype but shows essential Cdh1 function during placentation

Stemmler

Bedzhov

2010

Developmental Dynamics

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The specific roles of classical cadherins at key morphogenetic events during development are still not fully understood. As part of a project to study cadherin function during early mammalian development, we generated mice carrying an HA-epitope tagged Cdh1 (E-cadherin) cDNA knocked into the Cdh1 locus, similar to the previously described mouse mutants in which we forced Cdh2 (N-cadherin) expression in the Cdh1 expression domain. As expected and in contrast to Cdh1Cdh2/Cdh2 and Cdh1 2/2, our Cdh1HA/HA mutant embryos form proper trophectoderm, implant and undergo both gastrulation and neurulation. However, Cdh1 HA/HA mice display an unexpected phenotype at embryonic day 10.5. Cdh1 HA/HA embryos are smaller, paler and suffer from an insufficient nutrient supply. We detected a reduced expression of Cdh1 HA specifically in the extraembryonic ectoderm and in the labyrinth layer, whereas expression in the embryo proper was normal. With this approach, we show for the first time that Cdh1 is essential for the correct formation of the placenta. Placentas without Cdh1 expression are impaired and incapable of establishing a proper connection between the embryonic and the maternal blood vessels for efficient nutrient and oxygen transport. Developmental Dynamics 239:2330-2344,

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Section: Discussionsupporting

confidence: 60%

A Cdh1^HA knock‐in allele rescues the Cdh1^−/− phenotype but shows essential Cdh1 function during placentation

Stemmler

Bedzhov

2010

Developmental Dynamics

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“…It would be expected that fetal growth rates are also reduced. Fetal growth rates could be further impacted upon if placental growth rates were altered; a small placenta often times lead to placental insufficiency, the leading cause of intrauterine growth restriction (IUGR) [63][64][65]. The ability to maintain placental growth rates through a constant supply of membrane components could be a novel way to ensure adequate placental, and thereby fetal, growth rates.…”

Section: Discussionmentioning

confidence: 99%

Inability to fully suppress sterol synthesis rates with exogenous sterol in embryonic and extraembyronic fetal tissues

Yao

Jenkins

Horn

et al. 2007

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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SUMMARYThe requirement for cholesterol is greater in developing tissues (fetus, placenta, and yolk sac) as compared to adult tissues. Here, we compared cholesterol-induced suppression of sterol synthesis rates in the adult liver to the fetal liver, fetal body, placenta, and yolk sac of the Golden Syrian hamster. Sterol synthesis rates were suppressed maximally in non-pregnant adult livers when cholesterol concentrations were increased. In contrast, sterol synthesis rates were suppressed only marginally in fetal livers, fetal bodies, placentas, and yolk sacs when cholesterol concentrations were increased. To begin to elucidate the mechanism responsible for the blunted response of sterol synthesis rates in fetal tissues to exogenous cholesterol, the ratio of sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) to Insig-1 was measured in these same tissues since the ratio of SCAP to the Insigs can impact SREBP processing. The fetal tissues had anywhere from a 2-to 6-fold greater ratio of SCAP to Insig-1 than did the adult liver, suggesting constitutive processing of the SREBPs. As expected, the level of mature, nuclear SREBP-2 was not different in the fetal tissues with different levels of cholesterol whereas it was different in adult livers. These findings indicate that the suppression of sterol synthesis to exogenous sterol is blunted in developing tissues and the lack of response appears to be mediated at least partly through relative levels of Insigs and SCAP.

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“…Placental factors and hypoxemia are keys to intrauterine growth restriction (IUGR) and fetal death. IUGR is a condition associated with placental insufficiency (1). Adaptive changes in IUGR may fail at some point, leading to fetal death.…”

Section: Introductionmentioning

confidence: 99%

Histopathological analysis of the placental lesions in pregnancies complicated with IUGR and stillbirths in comparison with noncomplicated pregnancies

Günyeli¹,

Erdemoğlu²,

Ceylaner³

et al. 2011

J Turkish German Gynecol Assoc

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Placental-fetal Interrelationship in IUGR Fetuses—A Review

Cited by 250 publications

References 25 publications

A Cdh1^HA knock‐in allele rescues the Cdh1^−/− phenotype but shows essential Cdh1 function during placentation

A Cdh1^HA knock‐in allele rescues the Cdh1^−/− phenotype but shows essential Cdh1 function during placentation

Inability to fully suppress sterol synthesis rates with exogenous sterol in embryonic and extraembyronic fetal tissues

Histopathological analysis of the placental lesions in pregnancies complicated with IUGR and stillbirths in comparison with noncomplicated pregnancies

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Placental-fetal Interrelationship in IUGR Fetuses—A Review

Cited by 250 publications

References 25 publications

A Cdh1HA knock‐in allele rescues the Cdh1−/− phenotype but shows essential Cdh1 function during placentation

A Cdh1HA knock‐in allele rescues the Cdh1−/− phenotype but shows essential Cdh1 function during placentation

Inability to fully suppress sterol synthesis rates with exogenous sterol in embryonic and extraembyronic fetal tissues

Histopathological analysis of the placental lesions in pregnancies complicated with IUGR and stillbirths in comparison with noncomplicated pregnancies

Contact Info

Product

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A Cdh1^HA knock‐in allele rescues the Cdh1^−/− phenotype but shows essential Cdh1 function during placentation

A Cdh1^HA knock‐in allele rescues the Cdh1^−/− phenotype but shows essential Cdh1 function during placentation