Progressive uterine artery occlusion in the Guinea pig leads to defects in placental structure that relate to fetal growth

López-Tello, Jorge; Jiménez-Martínez, María Ángeles; Herrera, Emílio; Krause, Bernardo J.; Sferruzzi‐Perri, Amanda N.

doi:10.1016/j.placenta.2018.10.003

Cited by 16 publications

(10 citation statements)

References 32 publications

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“…The placental weight is closely related to poor fetal prognosis (24), and the placental volume is an independent predictor of fetal growth retardation (25). In this study, the results showed PDE declined the placental volume (Figure 2A,B, P<0.01) and weight (Figure 2C, P<0.05) in dosedependent manners.…”

Section: Decreased Placental Weight and Volume After Pdesupporting

confidence: 51%

Prenatal dexamethasone exposure exerts sex-specific effect on placental oxygen and nutrient transport ascribed to the differential expression of IGF2

Guo¹,

Fang²,

Zhuang³

et al. 2020

Ann Transl Med

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Background: Clinical studies have showed that dexamethasone exposure during pregnancy could cause fetal growth retardation, but the mechanism by which prenatal dexamethasone exposure influences placental nutrient transport is still unclear. This study investigated the impacts of prenatal dexamethasone on the placental oxygen and nutrient transport.Methods: Pregnant Wistar rats were subcutaneously administered with dexamethasone from day 9 to day 20 of gestation at 0.2 or 0.8 mg/kg•d. Pregnant rats were sacrificed on gestational day 20. The placental tissue was collected for analysis.Results: Prenatal dexamethasone exposure (PDE) declined the fetal weight and increased the intrauterine growth retardation (IUGR) rate in a dose-dependent manner. The total placental volume and the length, density and surface area of fetal capillaries in the labyrinth zone reduced in a dose-dependent manner. In addition, the thickness of syncytial membrane dose-dependently increased, resulting in a dose-dependent decrease in oxygen diffusion capacity. Furthermore, after PDE, the nutrient transport area and oxygen diffusion capacity of male placenta were lower than that of female placenta. The mRNA and protein expression of placental nutrient transporters including glucose transporter 1 (GLUT1), glucose transporter 3 (GLUT3), L-type amino acid transporter 1 (LAT1), lipoprotein lipase (LPL) and scavenger receptor class B type 1 (SRB1) increased in female placenta. However, in male placenta, the expression of LAT1, LPL and SRB1 was significantly decreased and GLUT1 and GLUT3 have a decrease trend. We further investigated the expression of insulin-like growth factor 1 (IGF1) and insulin-like growth factor 2 (IGF2) related to placental and fetal growth and development. Our study showed that the expression of IGF1 was significantly decreased both in male and female placentas after PDE. But the expression of IGF2 was significantly increased in female placentas while significantly decreased in male placentas. Conclusions:Our study shows prenatal dexamethasone exposure exerts sex-specific influence on the placental oxygen and nutrient transport. This might be ascribed to the differential expression of IGF2 after PDE. These findings provide evidence on the dexamethasone-induced toxicity to the placenta and fetal development.

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Section: Decreased Placental Weight and Volume After Pdesupporting

confidence: 51%

Prenatal dexamethasone exposure exerts sex-specific effect on placental oxygen and nutrient transport ascribed to the differential expression of IGF2

Guo¹,

Fang²,

Zhuang³

et al. 2020

Ann Transl Med

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“…The ligature of uterine vessels that supply the placenta (uteroplacental vessels) reduces both oxygen and nutrient supply and is an established method to induce IUGR in rats (Sferruzzi-Perri & Camm, 2016), guinea pigs (Lopez-Tello, Jimenez-Martinez, Herrera, Krause, & Sferruzzi-Perri, 2018), and rabbits (Eixarch et al, 2009(Eixarch et al, , 2011Flake et al, 1987;Flake, Villa-Troyer, Adzick, & Harrison, 1986;Harel et al, 1985). The procedure in rabbits is usually performed during the last third of gestation (GD21 or GD25) and the percentage of uteroplacental vessels ligated varies from 20%-50%.…”

Section: Utero-placental Vessel Ligationmentioning

confidence: 99%

Models of Intrauterine growth restriction and fetal programming in rabbits

López-Tello

Álvarez

González-Bulnes³

et al. 2019

Molecular Reproduction Devel

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Intrauterine growth restriction (IUGR) affects approximately 10% of human pregnancies globally and has immediate and life‐long consequences for offspring health. However, the mechanisms underlying the pathogenesis of IUGR and its association with later health and disease outcomes are poorly understood. To address these knowledge gaps, the use of experimental animals is critically important. Since the 50's different environmental, pharmacological, and surgical manipulations have been performed in the rabbit to improve our knowledge of the control of fetal growth, fetal responses to IUGR, and mechanisms by which offspring may be programmed by an adverse gestational environment. The purpose of this review is therefore to summarize the utility of the rabbit as a model for IUGR research. It first summarizes the knowledge of prenatal and postnatal development in the rabbit and how these events relate to developmental milestones in humans. It then describes the methods used to induce IUGR in rabbits and the knowledge gained about the mechanisms determining prenatal and postnatal outcomes of the offspring. Finally, it discusses the application of state of the art approaches in the rabbit, including high‐resolution ultrasound, magnetic resonance imaging, and gene targeting, to gain a deeper integrative understanding of the physiological and molecular events governing the development of IUGR. Overall, we hope to engage and inspire investigators to employ the rabbit as a model organism when studying pregnancy physiology so that we may advance our understanding of mechanisms underlying IUGR and its consequences in humans and other mammalian species.

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“…Morphology of the labyrinth region was assessed by double-labelling placental sections with rabbit antibodies against cytokeratin (180059, Thermo-Fisher Scientific, UK) and laminin (ab11575, abcam, UK) to identify trophoblast and fetal capillaries, respectively as previously described 73 . Slides were dewaxed, rehydrated and endogenous peroxidase quenched by incubation in 3% (v/v) hydrogen peroxide for 10 min.…”

Section: Methodsmentioning

confidence: 99%

Advanced maternal age compromises fetal growth and induces sex-specific changes in placental phenotype in rats

Napso

Hung

Davidge

et al. 2019

Sci Rep

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Advanced maternal age is associated with an increased risk of pregnancy complications. It programmes sex-specific cardiovascular dysfunction in rat offspring, however the intrauterine mechanisms involved remain unknown. This study in the rat assessed the impact of advanced maternal age on placental phenotype in relation to the growth of female and male fetuses. We show that relative to young (3–4 months) dams, advanced maternal age (9.5–10 months) compromises growth of both female and male fetuses but affects the placental phenotype sex-specifically. In placentas from aged versus young dams, the size of the placental transport and endocrine zones were increased and expression of Igf2 (+41%) and placental lactogen (Prl3b1: +59%) genes were upregulated in female, but not male fetuses. Placental abundance of IGF2 protein also decreased in the placenta of males only (−95%). Moreover, in placentas from aged versus young dams, glucocorticoid metabolism (11β-hsd2: +63% and 11β-hsd1: −33%) was higher in females, but lower in males (11β-hsd2: −50% and 11β-hsd1: unaltered). There was however, no change in the placental abundance of 11β-HSD2 protein in aged versus young dams regardless of fetal sex. Levels of oxidative stress in the placenta were increased in female and male fetuses (+57% and +90%, respectively) and apoptosis increased specifically in the placenta of males from aged rat dams (+700%). Thus, advanced maternal age alters placental phenotype in a sex-specific fashion. These sexually-divergent changes may play a role in determining health outcomes of female and male offspring of aged mothers.

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Progressive uterine artery occlusion in the Guinea pig leads to defects in placental structure that relate to fetal growth

Cited by 16 publications

References 32 publications

Prenatal dexamethasone exposure exerts sex-specific effect on placental oxygen and nutrient transport ascribed to the differential expression of IGF2

Prenatal dexamethasone exposure exerts sex-specific effect on placental oxygen and nutrient transport ascribed to the differential expression of IGF2

Models of Intrauterine growth restriction and fetal programming in rabbits

Advanced maternal age compromises fetal growth and induces sex-specific changes in placental phenotype in rats

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