At Term, XmO and XpO Mouse Placentas Show Differences in Glucose Metabolism in the Trophectoderm-Derived Outer Zone

He, Nannan; Lim, Shujing Jane; Mello, Joana Carvalho Moreira de; Navarro, I Blanco; Bialecka, Monika; Salvatori, Daniela; Westerlaken, Lucette A. J. van der; Pereira, Lygia V.; Lopes, Susana M. Chuva de Sousa

doi:10.3389/fcell.2017.00063

Cited by 6 publications

(3 citation statements)

References 64 publications

(76 reference statements)

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“…In extraembryonic lineages of female mouse conceptuses, the paternally inherited X-chromosome is preferentially silenced (Takagi & Sasaki 1975). A role for X-linked genes in regulating placental glycogen storage is demonstrated by mice that inherited only a single paternally inherited X chromosome (XpO) and display an expansion of the GlyT population (He et al 2017). In support of this hypothesis, GlyT phenotypes were reported to varying degrees in loss-of-function models of four X-linked genes (i.e.…”

Section: Imprinted and X-linked Genesmentioning

confidence: 95%

Placental glycogen stores and fetal growth: insights from genetic mouse models

Tunster¹,

Watson²,

Fowden³

et al. 2020

Reproduction

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The placenta performs a range of crucial functions that support fetal growth during pregnancy, including facilitating the supply of oxygen and nutrients to the fetus, removal of waste products from the fetus and the endocrine modulation of maternal physiology. The placenta also stores glucose in the form of glycogen, the function of which remains unknown. Aberrant placental glycogen storage in humans is associated with maternal diabetes during pregnancy and pre-eclampsia, thus linking placental glycogen storage and metabolism to pathological pregnancies. To understand the role of placental glycogen in normal and complicated pregnancies, we must turn to animal models. Over 40 targeted mutations in mice demonstrate the defects in placental cells that store glycogen and suggest that placental glycogen represents a source of readily mobilized glucose required during periods of high fetal demand. However, direct functional evidence is currently lacking. Here, we evaluate these genetic mouse models with placental phenotypes that implicate glycogen trophoblast cell differentiation and function to illuminate the common molecular pathways that emerge and to better understand the relationship between placental glycogen and fetal growth. We highlight the current limitations in exploring the key questions regarding placental glycogen storage and metabolism and define how to experimentally overcome these constraints.

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Section: Imprinted and X-linked Genesmentioning

confidence: 95%

Placental glycogen stores and fetal growth: insights from genetic mouse models

Tunster¹,

Watson²,

Fowden³

et al. 2020

Reproduction

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show abstract

“…Periodic Acid Schiff stain was used in this study to detect the amount of the glycogen in the tissue samples, and was quantified using the Image J software. The software has been used in numerous studies to quantify PAS staining in animal placentas (Rampon, et al [9] , He, et al [10] ). The current study classified PAS staining data into the five categories (Hazy, Traces, Mild, Moderate and Strong).…”

Section: Discussionmentioning

confidence: 99%

Histochemical Study of Human Placental Tissues in Gestational Diabetic Mellitus

Lafta

Abdulhameed

Al-Bakri

2021

IJEIR

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Gestational diabetes mellitus (GDM) is a serious pregnancy complication in which a woman who has never had diabetes develops chronic hyperglycemia during her pregnancy. Normal placental function is essential for optimal fetal growth. The transport of glucose from the mother to the fetus is critical for fetal nutrient demands and can be stored as glycogen in the placenta. However, the function of this glycogen deposition is unknown: It may well be a source of fuel for a placenta itself or the storage reservoir for the later use by the fetus in times of need. While the significance of the placental glycogen remains unknown, the mounting evidence indicates that the altered glycogen metabolism and/or deposition is associated with many pregnancy complications, such as gestational diabetes, that adversely affect fetal development. The aim of this study is to assess glycogen deposition using Histochemical staining of Periodic Acid Schiff (PAS) stain. The placenta tissue collected from 50 women were enrolled in this study (25 women with no complications) and (25 women with gestational diabetes). The placentas of the two groups were compared in this study based on glycogen deposition with periodic acid-Schiff stain. The results of a histochemical investigation using PAS stain revealed a significant increase in the glycogen deposition (p≤0.001) in diabetic women's placentas within the intervillous core, around fetal vessels, and the basement membranes.

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“…Glycogen trophoblast cells accumulate glycogen within their cytoplasm beginning at approximately embryonic Day 12.5, and mainly provide energy for the next stage of pregnancy (Coan, Conroy, Burton, & Ferguson-Smith, 2006). Previous reports have shown that abnormal glycogen trophoblast cell numbers might be related to impaired glucose transport and glycogen metabolism in the placenta (Bogutz et al, 2018;N. He et al, 2017;Sibley et al, 2004).…”

Section: Tissue Expression Enrichment Analysismentioning

confidence: 99%

Deletion of Prl7d1 causes placental defects at mid‐pregnancy in mice

Zhang

Hao

2019

Molecular Reproduction Devel

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Prolactin family 7, subfamily d, member 1 (Prl7d1), a member of the expanding prolactin family, is mainly expressed in the placental junctional zone (including trophoblast giant cells and spongiotrophoblast cells) with peak expression observed at 12 days postcoitum (dpc) in mice. Previous studies have shown that PRL7D1 is a key mediator of angiogenesis in vitro; however, its physiological roles in placental development in vivo have not been characterized. To address this issue, we deleted Prl7d1 in mice and demonstrated that its absence results in reduced litter size and fertility. Histologically, Prl7d1 mutants exhibited striking placental abnormalities at 12.5 dpc, including a reduction in the proportion of labyrinth layers and a significant increase in decidual natural killer cells, glycogen trophoblasts, and trophoblast giant cells in the junctional zone. Moreover, placentas from Prl7d1‐null mice displayed a thickened decidual spiral artery. Notably, these negative effects were more pronounced in male fetuses. Further RNA‐sequencing analysis showed that Prl7d1 deletion results in significant differences in the placental transcriptome profile between the two sexes of fetuses. Together, this study demonstrates that Prl7d1 possesses antiangiogenic properties in deciduas and inhibits the development of junctional zone, which potentially alters the functional capacity of the placenta to support optimal fetal growth. Moreover, of note, the role of Prl7d1 in the placenta is regulated in a fetal sex‐specific manner.

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At Term, XmO and XpO Mouse Placentas Show Differences in Glucose Metabolism in the Trophectoderm-Derived Outer Zone

Cited by 6 publications

References 64 publications

Placental glycogen stores and fetal growth: insights from genetic mouse models

Placental glycogen stores and fetal growth: insights from genetic mouse models

Histochemical Study of Human Placental Tissues in Gestational Diabetic Mellitus

Deletion of Prl7d1 causes placental defects at mid‐pregnancy in mice

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