Notch2 is required for formation of the placental circulatory system, but not for cell-type specification in the developing mouse placenta

Hamada, Y.; Hiroe, Takeshi; Oda, Mayumi; Tsujimoto, Yoshihide; Coleman, John R.; Tanaka, Satoshi

doi:10.1111/j.1432-0436.2006.00137.x

Cited by 28 publications

(22 citation statements)

References 50 publications

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“…Notch2 function is required for mouse placental development (Hamada et al, 2007). Tetraploid complementation, in which Notch2-deficient embryos were provided with wild-type placentas, revealed placental insufficiency as the primary cause of lethality.…”

Section: Discussionmentioning

confidence: 99%

“…As to function, Notch2, Hes2 and Hes3 are co-expressed in trophoblast giant cells (TGCs), which, along with glycogen trophoblast cells (GlyTCs), carry out interstitial and endovascular invasion. Tetraploid rescue experiments in Notch2-deficient mice revealed that placental defects involving the labyrinthian circulatory system are associated with the lethality in Notch2-deficient animals (Hamada et al, 2007). However, the mechanisms involved remained elusive.…”

Section: Introductionmentioning

confidence: 99%

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A role for Notch signaling in trophoblast endovascular invasion and in the pathogenesis of pre-eclampsia

et al. 2011

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SUMMARYPlacental trophoblasts (TBs) invade and remodel uterine vessels with an arterial bias. This process, which involves vascular mimicry, re-routes maternal blood to the placenta, but fails in pre-eclampsia. We investigated Notch family members in both contexts, as they play important roles in arterial differentiation/function. Immunoanalyses of tissue sections showed step-wise modulation of Notch receptors/ligands during human TB invasion. Inhibition of Notch signaling reduced invasion of cultured human TBs and expression of the arterial marker EFNB2. In mouse placentas, Notch activity was highest in endovascular TBs. Conditional deletion of Notch2, the only receptor upregulated during mouse TB invasion, reduced arterial invasion, the size of maternal blood canals by 30-40% and placental perfusion by 23%. By E11.5, there was litter-wide lethality in proportion to the number of mutant offspring. In pre-eclampsia, expression of the Notch ligand JAG1 was absent in perivascular and endovascular TBs. We conclude that Notch signaling is crucial for TB vascular invasion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A role for Notch signaling in trophoblast endovascular invasion and in the pathogenesis of pre-eclampsia

et al. 2011

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“…Notch2 deletion results in embryonic lethality at E11.5 (Hamada Notch signalling during embryo implantation R81 et al 1999). Hamada et al 2007 demonstrated that whole embryo culture evaded lethality in mutant embryos, suggesting an extraembryonic cause. Notch2 localizes to maternal sinusoidal trophoblasts in the mouse placental labyrinth, the site of fetal-maternal exchange, and from the histology of early Notch2-deficient placentas, poor maternal blood sinus formation was evident (Hamada et al 2007).…”

Section: Notch Signalling In the Mouse Placentamentioning

confidence: 99%

“…Hamada et al 2007 demonstrated that whole embryo culture evaded lethality in mutant embryos, suggesting an extraembryonic cause. Notch2 localizes to maternal sinusoidal trophoblasts in the mouse placental labyrinth, the site of fetal-maternal exchange, and from the histology of early Notch2-deficient placentas, poor maternal blood sinus formation was evident (Hamada et al 2007). More recently, conditional deletion under the Tpbpa promoter (Simmons et al 2007) specific for invasive spiral arteriole giant trophoblast Cell (TGC) and glycogen trophoblast cell lineages has shown impaired trophoblast invasion into the maternal arteries and reduced maternal canal size and placental perfusion (Hunkapiller et al 2011).…”

Section: Notch Signalling In the Mouse Placentamentioning

confidence: 99%

Fetal–maternal communication: the role of Notch signalling in embryo implantation

Cuman¹,

Menkhorst²,

Winship³

et al. 2014

Reproduction

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The establishment of a successful pregnancy requires the implantation of a competent blastocyst into a 'receptive' endometrium, facilitating the formation of a functional placenta. Inadequate or inappropriate implantation and placentation is a major reason for infertility and is thought to lead to first-trimester miscarriage, placental insufficiency and other obstetric complications. Blastocystendometrial interactions are critical for implantation and placental formation. The Notch signalling family is a receptor-ligand family that regulates cellular processes as diverse as proliferation, apoptosis, differentiation, invasion and adhesion. Notch signalling is achieved via cell-cell interaction; thus, via Notch, cells can have direct effects on the fate of their neighbours. Recently, a number of studies have identified Notch receptors and ligands in the endometrium, blastocyst and placenta. This review collates current knowledge of this large receptor-ligand family and explores the role of Notch signalling during implantation and placentation, drawing on information from both human and animal studies. Overall, the evidence suggests that Notch signalling is a critical component of fetal-maternal communication during implantation and placentation and that abnormal Notch expression is associated with impaired placentation and pre-eclampsia.Reproduction (2014) 147 R75-R86

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“…In the human placenta, the expression patterns of Notch1, Notch4, and Jag1 indicate a potential role for Notch signaling in placenta angiogenesis [14]. Further the Notch signal pathway also takes part in the processes of angiogenesis and arteriogenesis in mouse placenta formation [15,16].…”

Section: Introductionmentioning

confidence: 99%

Notch1Signaling Antagonizes Transforming Growth Factor-β Pathway and Induces Apoptosis in Rabbit Trophoblast Stem Cells

Tan

Lü

Zhang

et al. 2014

Stem Cells and Development

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Notch2 is required for formation of the placental circulatory system, but not for cell-type specification in the developing mouse placenta

Cited by 28 publications

References 50 publications

A role for Notch signaling in trophoblast endovascular invasion and in the pathogenesis of pre-eclampsia

A role for Notch signaling in trophoblast endovascular invasion and in the pathogenesis of pre-eclampsia

Fetal–maternal communication: the role of Notch signalling in embryo implantation

Notch1Signaling Antagonizes Transforming Growth Factor-β Pathway and Induces Apoptosis in Rabbit Trophoblast Stem Cells

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