The hemo‐chorial mouse placenta

Kirby, D. R. S.; Bradbury, S.

doi:10.1002/ar.1091520307

Cited by 43 publications

(16 citation statements)

References 11 publications

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“…4 a and b), or gene expression markers such as Igf2 (27,28). With the use of all three assays, it was found that in the pUPD12 junctional zone, ''glycogen'' cells are more abundant than normal at E13.5 and E15.5 (data not shown), and their dramatic -t3), the fetal capillary endothelium (fc), and its associated basement membrane (bm) in the normal feto-maternal interface (e) as shown previously (25,26). The outermost trophoblast layer (t3), which is cytotrophoblastic (25), is loosely attached to the middle layer (t2), which is syncytial (25).…”

Section: Resultssupporting

confidence: 59%

“…The labyrinth is the zone where fetal blood and maternal blood circulate within fetal capillaries and maternal blood spaces, respectively, for physiological exchange through zygote-derived feto-maternal interfaces (1,2,(24)(25)(26). These labyrinthine interfaces consist of the endothelial cells of fetal capillaries, their associated basement membrane, and a trilaminar layer of trophoblast cells that directly lines the maternal blood spaces (25,26) (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Roles for genomic imprinting and the zygotic genome in placental development

Georgiades

Watkins

Burton

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

130

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The placenta contains several types of feto-maternal interfaces where zygote-derived cells interact with maternal cells or maternal blood for the promotion of fetal growth and viability. The genetic factors regulating the interactions between different cell types within fetomaternal interfaces and the relative contributions of the maternal and zygotic genomes are poorly understood. Genomic imprinting, the epigenetic process responsible for parental origin-dependent functional differences between homologous chromosomes, has been proposed to contribute to these events. Previous studies showed that mouse conceptuses with an absence of imprinted differences between the two copies of chromosome 12 (upon paternal inheritance of both copies) die late in gestation and have a variety of defects, including placentomegaly. Here we examined the role of chromosome 12 imprinting in these placentae in more detail. We show that the spatial interactions between different cell types within fetomaternal interfaces are defective and identify abnormal behaviors in both zygote-derived and maternal cells that are attributed to the genome of the zygote but not the mother. These include compromised invasion of the maternal decidualized endometrium and the central maternal artery situated within it by zygote-derived trophoblast, abnormalities in the wall of the central maternal artery, and defects within the zygote-derived cellular layer of the labyrinth, which is in direct contact with maternal blood. These findings demonstrate multiple roles for chromosome 12 imprinting in the placenta that have not previously been associated with imprinting effects. They provide insights into the function of imprinting in placental development and have evolutionary and clinical implications.

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Section: Resultssupporting

confidence: 59%

Section: Resultsmentioning

confidence: 99%

Roles for genomic imprinting and the zygotic genome in placental development

Georgiades

Watkins

Burton

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

130

View full text Add to dashboard Cite

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“…The placentas of monkeys, lambs, pigs, goats, rats, and mice have each been studied as models of human placental structure and function, but there are significant differences among their macro-and microstructures that must be considered (174,311,536,553,575,644).…”

Section: Placental Structure and Expression Of Calciotropic And Phospmentioning

confidence: 99%

“…B) HUMAN DATA. Human placentas are discoid and hemochorial and are considered to have similar structure, function, and diffusional characteristics to placentas of mice and rats (174,311,536,553). They are hemomonochorial, meaning that a single trophoblast cell layer separates maternal and fetal blood.…”

Section: Placental Structure and Expression Of Calciotropic And Phospmentioning

confidence: 99%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

211

188

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Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

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“…4L). The fetal vasculature in the labyrinth, which is separated by the trophoblast layers from maternal blood sinuses, undergoes rapid growth during placenta development (Kirby and Bradbury, 1965). Thus, while VEGFRY flk-1 expressing cells were in proximity of the VEGF producing cells, the VEGFRl/flt-1 expressing cells were located at a relatively high distance.…”

Section: Expression Of Vegfruflt-1 During Vasculogenesis and During Pmentioning

confidence: 99%

Coordinate expression of vascular endothelial growth factor receptor‐1 (fit‐1) and its ligand suggests a paracrine regulation of murine vascular development

Breier

Clauss

Risau

1995

Developmental Dynamics

281

152

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Vascular endothelial growth factor (VEGF) is a candidate regulator of blood vessel growth during embryonic development and in tumors. To evaluate the role of VEGF receptor-l/ flt-1 (VEGFRl/flt-1) in the development of the vascular system, we have characterized the murine homolog of the human flt-1 gene and have analyzed its expression pattern during mouse embryogenesis. Receptor binding studies using transfected COS cells revealed that the murine flt-1 gene encodes a high affinity receptor for VEGF. The apparent K, for VEGF binding, as determined by Scatchard analysis, was 114 pM, demonstrating that VEGFRl/flt-1 has a higher affinity to VEGF than VEGF receptor-2/flk-l (VEGFR2/flk-l). By in situ hybridization, VEGFRl/flt-1 was detected in the yolk sac mesoderm already at the early stages of vascular development, while the receptor ligand was expressed in the entire endoderm of 7.5-day mouse embryos. A comparison with VEGFR2/flk-1 showed that the two receptors shared a common expression domain in the yolk sac mesoderm, but were expressed at different sites in the ectoplacental cone. The differential expression of the two VEGF receptors persisted in the developing placenta, where VEGFRl/flt-1 mRNA was detected in the spongiotrophoblast layer, whereas VEGFR2/ flk-1 transcripts were present in the labyrinthine layer which is the site of VEGF expression. In the embryo proper, VEGFRlIflt-1 mRNA was specifically localized in blood vessels and capillaries of the developing organs, closely resembling the pattern of VEGFR2/flk-1 transcript distribution. In the developing brain, the expression of VEGF receptors in the perineural capillary plexus and in capillary sprouts which have invaded the neuroectoderm correlated with endothelial cell proliferation and brain angiogenesis. The data are consistent with the hypothesis that VEGF and its receptors have an important function both in the differentiation of the endothelial lineage and in the neovascularization of developing organs, and act in a paracrine fashion. o 1995 Wiley-Liss, Inc.

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The hemo‐chorial mouse placenta

Cited by 43 publications

References 11 publications

Roles for genomic imprinting and the zygotic genome in placental development

Roles for genomic imprinting and the zygotic genome in placental development

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Coordinate expression of vascular endothelial growth factor receptor‐1 (fit‐1) and its ligand suggests a paracrine regulation of murine vascular development

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