Histological study of the materno-embryonic interface in spontaneous abortion

Hustin, J.; Jauniaux, Eric; Schaaps, Jean-Pierre

doi:10.1016/s0143-4004(05)80193-6

Cited by 281 publications

(149 citation statements)

References 10 publications

Supporting

Mentioning

139

Contrasting

Unclassified

Order By: Relevance

“…The blood vessel walls are remodeled by this invasion at the maternal-fetal interface to provide sufficient nutrients and oxygen for the fetus [3,4]. Impaired invasion of trophoblast cells into the maternal tissue or insufficient uterine spiral artery remodeling may lead to preeclampsia (PE) [2,5], intrauterine growth restriction [6] and other obstetric complications [7,8]. The detailed molecular mechanism involved in regulating trophoblast invasion requires further elucidation.…”

Section: Introductionmentioning

confidence: 99%

N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy

et al. 2015

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy

et al. 2015

View full text Add to dashboard Cite

show abstract

“…The latter deeply migrate into uterine tissue and the maternal spiral arteries, provoking vessel remodelling and adaptation of adequate blood flow to the placenta (5,6). Failures in placentation and artery remodelling have been associated with a variety of pregnancy diseases, such as miscarriage, preeclampsia, fetal growth restriction, and preterm labor (7)(8)(9)(10). Besides unfavorable immunological interactions of EVTs with uterine natural killer (uNK) cells (11), abnormal placental development and trophoblast differentiation are thought to contribute to the pathogenesis of gestational disorders.…”

mentioning

confidence: 99%

Notch1 controls development of the extravillous trophoblast lineage in the human placenta

Haider

Meinhardt

Saleh

et al. 2016

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

124

144

View full text Add to dashboard Cite

Development of the human placenta and its different epithelial trophoblasts is crucial for a successful pregnancy. Besides fusing into a multinuclear syncytium, the exchange surface between mother and fetus, progenitors develop into extravillous trophoblasts invading the maternal uterus and its spiral arteries. Migration into these vessels promotes remodelling and, as a consequence, adaption of blood flow to the fetal–placental unit. Defects in remodelling and trophoblast differentiation are associated with severe gestational diseases, such as preeclampsia. However, mechanisms controlling human trophoblast development are largely unknown. Herein, we show that Notch1 is one such critical regulator, programming primary trophoblasts into progenitors of the invasive differentiation pathway. At the 12th wk of gestation, Notch1 is exclusively detected in precursors of the extravillous trophoblast lineage, forming cell columns anchored to the uterine stroma. At the 6th wk, Notch1 is additionally expressed in clusters of villous trophoblasts underlying the syncytium, suggesting that the receptor initiates the invasive differentiation program in distal regions of the developing placental epithelium. Manipulation of Notch1 in primary trophoblast models demonstrated that the receptor promotes proliferation and survival of extravillous trophoblast progenitors. Notch1 intracellular domain induced genes associated with stemness of cell columns, myc and VE-cadherin, in Notch1−fusogenic precursors, and bound to themycpromoter and enhancer region at RBPJκ cognate sequences. In contrast, Notch1 repressed syncytialization and expression of TEAD4 and p63, two regulators controlling self-renewal of villous cytotrophoblasts. Our results revealed Notch1 as a key factor promoting development of progenitors of the extravillous trophoblast lineage in the human placenta.

show abstract

“…It has been suggested that it is necessary for embryo viability by ensuring undisturbed f low of maternal blood to the labyrinth due to the inability of the arterial wall to contract in response to vasomotor signals from the mother (1,32). This conclusion is supported by the findings that (i) experimentally induced temporal restriction of maternal blood through the rat central maternal artery on the fourth day before birth is associated with fetal death (35) and (ii) the absence of this arterial transformation in human placentae is associated with fetal death and other complications (7)(8)(9). The progressive lethality of pUPD12 embryos after E15.5 in the absence of any obvious embryonic defects that could be compatible with intrauterine death (15) is consistent with the theory that the absence of arterial wall transformation leads to embryonic lethality.…”

Section: Discussionmentioning

confidence: 84%

“…This change also occurs in humans and other mammals and is thought to free the artery from the vasomotor inf luences of the mother, thus allowing undisturbed maternal blood f low to the labyrinth (1,31,32). This physiological change is believed to be essential for the maintenance of a healthy pregnancy because its absence in humans is associated with fetal death and other pregnancy complications (7)(8)(9). The genetic basis of this maternal vasculature transformation and the role of the zygotic genome in this process are unknown.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

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

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.

show abstract

Histological study of the materno-embryonic interface in spontaneous abortion

Cited by 281 publications

References 10 publications

N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy

N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy

Notch1 controls development of the extravillous trophoblast lineage in the human placenta

Roles for genomic imprinting and the zygotic genome in placental development

Contact Info

Product

Resources

About