Development of Structures and Transport Functions in the Mouse Placenta

Watson, Erica D.; Cross, James C.

doi:10.1152/physiol.00001.2005

Cited by 494 publications

(549 citation statements)

References 109 publications

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“…Many genes are thought to be involved in the regulation of placental functions (Watson and Cross, 2005) but the molecular mechanisms are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Localization and subcellular distribution of prolyl oligopeptidase in the mouse placenta

2011

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Prolyl oligopeptidase (POP) is a serine endopeptidase which selectively digests a -Pro-X-peptide bond.Our previous study showed that POP mRNA was strongly expressed in the spongiotrophoblast of the mouse placenta at E17.5, suggesting its importance in development. To gain more insight into POP's role during gestation, we investigated its expression using different developmental stages of placenta. As a result of in situ hybridization, we found that localization of POP mRNA changed at E12.5. POP mRNA was strongly expressed in the spongiotrophoblast and labyrinth at E10.5 and E11.5 but thereafter only in the spongiotrophoblast. Immunohistochemistry revealed that POP was present in the parietal trophoblast giant cell, the spongiotrophoblast cell, and the labyrinth at E11.5 but the strong expression in the labyrinth was maintained only in the canal-associated and sinusoidal trophoblast giant cells at E16.5 and E18.5. To determine subcellular distribution of the POP protein, we fractionated the placental extract into cytoplasmic, membrane, and nuclear subfractions. By Western blot analysis, POP was detected in the cytoplasmic and membrane fractions but not in the nuclear fraction at E11.5 and E16.5. Interestingly, the cytoplasmic POP exhibited higher enzymatic activity than the membrane-associated type. These data suggest that the cytoplasmic and membrane-associated POP have distinct roles in different types of placental cells.

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“…Many genes are thought to be involved in the regulation of placental functions (Watson and Cross, 2005) but the molecular mechanisms are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Localization and subcellular distribution of prolyl oligopeptidase in the mouse placenta

2011

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“…En effet, la délétion spécifique du gène b-Raf dans les cellules endothé-liales à l'aide de la lignée transgénique Tie2-Cre ou encore la délétion du gène Mek1 par la recombinase Sox2-Cre dans tous les tissus embryonnaires (incluant l'allantoïde), ne génère aucun défaut placentaire et adjacente à l'endothélium foetal. Les cellules sanguines maternelles et les érythrocytes foetaux sont donc séparés par une triple couche de cellules trophoblastiques du labyrinthe et par les cellules endothéliales foetales ( Figure 1B) [20,24]. Les S-TGC sont un sous-type de trophoblastes géants pourvus de fonctions endocrines.…”

Section: Distribution Spatiale Des Protéines Mek1 Et Mek2unclassified

“…Les S-TGC sont un sous-type de trophoblastes géants pourvus de fonctions endocrines. Les SynT-I et SynT-II sont des cellules postmitotiques multinucléées formées par fusion cellulaire et possédant des fonctions de transport [20,25]. Ainsi, des anomalies affectant les cellules trophoblastiques ou les cellules endothéliales issues de l'allantoïde peuvent mener à des problèmes de vascularisation placentaire.…”

Section: Distribution Spatiale Des Protéines Mek1 Et Mek2unclassified

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Le rôle des kinasesMek1etMek2dans la formation de la barrière hématoplacentaire chez la souris

2012

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> La voie de signalisation cellulaire ERK/MAPK (extracellular signal-regulated kinase/mitogenactivated protein kinase) est impliquée dans plusieurs fonctions cellulaires. Chez la souris, l'invalidation de gènes codant pour des membres de cette voie est souvent associée à une mort embryonnaire consécutive à un développement anormal du placenta. Ce dernier est essentiel aux échanges nutritionnels et gazeux entre les circulations maternelle et embryonnaire, ainsi qu'à l'évacuation des déchets métaboliques. Ces échanges s'effectuent sans contact direct entre les deux circulations. Chez la souris, la barrière hématoplacentaire est constituée d'une triple couche de cellules trophoblastiques et de cellules endothéliales de l'embryon. MEK1 (ou MAP/ERK kinase-1) et MEK2 sont des kinases à double spécificité, phosphorylant les résidus sérine/thréonine et tyrosine et responsables de l'activation des kinases ERK1 et ERK2. L'inactivation génique de Mek1 produit une malformation placentaire résultant de défauts de prolifération et de différenciation des cellules trophoblastiques et entraînant un retard sévère du développement du placenta et la mort de l'embryon. Bien que les mutants Mek2 -/-survivent sans aucun phénotype apparent, les mutants doubles hétérozygotes Mek1 +/-Mek2 +/-meurent au cours de la gestation de malformation placentaire. L'ensemble de ces données souligne le rôle crucial de la voie ERK/MAPK dans la formation des structures extraembryonnaires. < cibles intracellulaires localisées dans la membrane plasmique, le cytoplasme, le cytosquelette ou le noyau [1,2]. Plusieurs cascades de signalisation MAPK ont été décrites chez les vertébrés. La voie classique ERK/MAPK constitue la voie majeure dans la réponse aux facteurs de croissance. Cette voie utilise les kinases régulées par les signaux extracellulaires, ERK1 et ERK2, ainsi que les kinases MEK1 et MEK2 à double spécificité (sérine/thréonine et tyrosine), qui activent ERK1 et ERK2 en réponse à la liaison de facteurs de croissance à leur récepteur. La voie ERK/MAPK est impliquée dans la détermination cellulaire chez plusieurs espèces. Chez les mammifères, cette cascade est impliquée dans la prolifération, la différenciation, la migration, la survie et la mort cellulaires [3,4]. La voie d'activation ERK/MAPK débute par la liaison de facteurs de croissance aux récepteurs membranaires à activité tyrosine kinase, tels les récepteurs du FGF (fibroblast growth factor), de l'EGF (epidermal growth factor) et du PDGF (platelet derived growth factor). Ces récepteurs s'activent par une autophosphorylation suivie du recrutement d'une protéine adaptatrice comme GRB2 (growth factor receptorbound protein 2) et l'interaction avec SOS-1 (son of sevenless homolog 1), un facteur d'échange de GDP/GTP de la petite protéine G RAS. SOS-1 permet le relargage du GDP associé à RAS qui peut alors fixer le GTP et s'activer. RAS activé permet le recrutement et l'activation de la kinase proto-oncogène RAF. Par la suite, les protéines kinases RAF, MEK et ERK s'activent séquentiellement par ph...

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“…The mouse placenta consists of three distinct layers, including the maternal layer (decidua), the junctional zone (where the placenta attaches to the uterus) and the labyrinth zone (where the placental villi are bathed in maternal blood and the site of maternal-fetal nutrient and oxygen exchange) 5 . Similar to the human placenta, the mouse placenta consists of highly specialized trophoblast cell types which have distinct roles in invading the maternal decidua, anchoring the placenta to the uterus and forming villi to facilitate nutrient transport.…”

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confidence: 99%

Zika virus — placental passage and permissivity for infection

Suter

Aagaard

2016

Nat Rev Endocrinol

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Zika virus (ZIKV) is an arbovirus that is transmitted to humans by the Aedes mosquito, but can be spread from one human to another, including fetal transmission during pregnancy. Infection of humans with ZIKV, an emerging mosquito-borne Flavivirus, has reached pandemic levels in the Americas, with at least 32 countries or territories reporting infection over the period May 2015 to April 2016 (REF. 1). Although previous outbreaks of ZIKV resembled that of dengue fever and chikungunya, its recent spread to the Americas has revealed an increase in the incidence of congenital microcephaly with brain and ocular malformations, as well as intrauterine growth restriction (IUGR) associated with placental insufficiency, and spontaneous pregnancy loss. As ZIKV RNA has been reported in amniotic fluid, the placenta and fetal neural tissue from women weeks to months after being infected early in gestation 2 , understanding the role of the placenta in alternately facilitating or limiting vertical transmission of ZIKV is of paramount importance. In a recent study published in Cell, Miner and colleagues describe two mouse models of ZIKV infection during pregnancy that are associated with clinically relevant phenotypes in offspring, including growth restriction and placental damage 3 .heterozygous offspring with an intact type I interferon response (Ifnar1 −/+ ). The pregnant Ifnar1 −/− mice were then inoculated with ZIKV on embryonic days 6.5 (E6.5) and E7.5, and pregnancy was allowed to progress until E13.5 or E15.5. The outcomes were devastating: the majority of fetuses were resorbed after in utero demise, similar to the observed pregnancy losses occurring in the current epidemic across the Americas. The remaining fetuses showed evidence of growth restriction and placental damage, including necrotic foci, but without evidence of microcephaly. However, in a second model of ZIKV infection in pregnancy, the investigators treated wild-type pregnant mice with an antibody targeting the IFN α/β receptor 1 1 day before infection with ZIKV at E6.5 and E7.5 and analysed phenotypes on E13.5 and E15.5. This second model was less severe than the first model, as prevalent fetal demise was not observed; however, the fetuses did exhibit IUGR.Despite the 6-8 day interval between initial infection and delivery of the fetuses, a high placental viral load was persistently observed. The mouse placenta consists of three distinct layers, including the maternal layer (decidua), the junctional zone (where the placenta attaches to the uterus) and the labyrinth zone (where the placental villi are bathed in maternal blood and the site of maternal-fetal nutrient and oxygen exchange) 5 . Similar to the human placenta, the mouse placenta consists of highly specialized trophoblast cell types which have distinct roles in invading the maternal decidua, anchoring the placenta to the uterus and forming villi to facilitate nutrient transport. In humans, the placenta has been observed to largely protect against vertical transmission of viruses, although some virus...

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Development of Structures and Transport Functions in the Mouse Placenta

Cited by 494 publications

References 109 publications

Localization and subcellular distribution of prolyl oligopeptidase in the mouse placenta

Localization and subcellular distribution of prolyl oligopeptidase in the mouse placenta

Le rôle des kinasesMek1etMek2dans la formation de la barrière hématoplacentaire chez la souris

Zika virus — placental passage and permissivity for infection

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