Intersection of Regulatory Pathways Controlling Hemostasis and Hemochorial Placentation [rat II]
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PROVIDER: PRJNA721710 | ENA |
REPOSITORIES: ENA
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Project description:Intersection of Regulatory Pathways Controlling Hemostasis and Hemochorial Placentation
| PRJNA721709 | ENA
Project description:Intersection of Regulatory Pathways Controlling Hemostasis and Hemochorial Placentation [human]
| PRJNA718820 | ENA
Project description:Intersection of Regulatory Pathways Controlling Hemostasis and Hemochorial Placentation [rat I]
| PRJNA721711 | ENA
Project description:Tissue factor pathway inhibitor (TFPI) is a prominent regulator of blood coagulation and an intriguing constituent of trophoblast cells situated at the maternal-fetal interface. The actions of TFPI extend beyond controlling hemostasis and directly affect trophoblast cell development. TFPI facilitates the differentiation of rat and human trophoblast stem cells into the invasive trophoblast/extravillous cell lineage and promotes intrauterine trophoblast invasion and trophoblast-guided uterine spiral artery remodeling at the maternal-fetal interface. Thus, TFPI is a conserved regulator of a fundamental event determining the efficacy of the hemochorial placenta.
2021-11-25 | GSE171223 | GEO
Project description:Tissue factor pathway inhibitor (TFPI) is a prominent regulator of blood coagulation and an intriguing constituent of trophoblast cells situated at the maternal-fetal interface. The actions of TFPI extend beyond controlling hemostasis and directly affect trophoblast cell development. TFPI facilitates the differentiation of rat and human trophoblast stem cells into the invasive trophoblast/extravillous cell lineage and promotes intrauterine trophoblast invasion and trophoblast-guided uterine spiral artery remodeling at the maternal-fetal interface. Thus, TFPI is a conserved regulator of a fundamental event determining the efficacy of the hemochorial placenta.
2021-11-25 | GSE171754 | GEO
Project description:Tissue factor pathway inhibitor (TFPI) is a prominent regulator of blood coagulation and an intriguing constituent of trophoblast cells situated at the maternal-fetal interface. The actions of TFPI extend beyond controlling hemostasis and directly affect trophoblast cell development. TFPI facilitates the differentiation of rat and human trophoblast stem cells into the invasive trophoblast/extravillous cell lineage and promotes intrauterine trophoblast invasion and trophoblast-guided uterine spiral artery remodeling at the maternal-fetal interface. Thus, TFPI is a conserved regulator of a fundamental event determining the efficacy of the hemochorial placenta.
2021-11-25 | GSE171753 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-11-26 | GSE171755 | GEO
Project description:AKT1 is a serine/threonine kinase implicated in fetal, placental, and postnatal growth. In this study, we investigated roles for AKT1 in placental development using a genome-edited/loss-of-function rat model. Both heterozygous and homozygous Akt1 mutant rats were viable and fertile. Disruption of AKT1 resulted in placental, fetal, and postnatal growth restriction. Akt1 null placentas showed deficits in both junctional zone and labyrinth zone size and their ability to adapt to a physiological stressor. Robust differences in the transcriptome of wild type versus Akt1 null junctional zones were identified. Among the differentially expressed junctional zone transcripts was forkhead box O4 (Foxo4), which encodes a transcription factor and known AKT substrate. FOXO4 expression was prominent in the junctional zone and invasive trophoblast cells of the rat placentation site and enhanced following rat TS cell differentiation. Foxo4 gene disruption using genome-editing resulted in placentomegaly, including an enlarged junctional zone. AKT1 and FOXO4 regulate the expression of many of the same transcripts expressed by trophoblast cells; however, in opposite directions. In summary, we have identified AKT1 and FOXO4 as part of a regulatory network controlling hemochorial placenta development.
2023-01-05 | GSE205829 | GEO
Project description:AKT1 is a serine/threonine kinase implicated in fetal, placental, and postnatal growth. In this study, we investigated roles for AKT1 in placental development using a genome-edited/loss-of-function rat model. Both heterozygous and homozygous Akt1 mutant rats were viable and fertile. Disruption of AKT1 resulted in placental, fetal, and postnatal growth restriction. Akt1 null placentas showed deficits in both junctional zone and labyrinth zone size and their ability to adapt to a physiological stressor. Robust differences in the transcriptome of wild type versus Akt1 null junctional zones were identified. Among the differentially expressed junctional zone transcripts was forkhead box O4 (Foxo4), which encodes a transcription factor and known AKT substrate. FOXO4 expression was prominent in the junctional zone and invasive trophoblast cells of the rat placentation site and enhanced following rat TS cell differentiation. Foxo4 gene disruption using genome-editing resulted in placentomegaly, including an enlarged junctional zone. AKT1 and FOXO4 regulate the expression of many of the same transcripts expressed by trophoblast cells; however, in opposite directions. In summary, we have identified AKT1 and FOXO4 as part of a regulatory network controlling hemochorial placenta development.
2023-01-05 | GSE205828 | GEO
Project description:Establishment of the hemochorial placentation site requires the exodus of trophoblast cells from the placenta and their transformative actions on the uterine vasculature, which is a critical but poorly understood developmental process. CBP/p300-interacting transactivator with glutamic acid/aspartic acid-rich carboxyl terminal domain 2 (CITED2) is a member of the CITED protein family of co-regulators and has been shown to possess roles in embryogenesis, including placenta development. We examined the involvement of CITED2 in the rat, which exhibits deep hemochorial placentation, a feature it shares with the human. CITED2 is distinctively expressed in the junctional zone compartment of the rat placentation site and in intrauterine invasive trophoblast cells. Homozygous disruption of the rat Cited2 locus resulted in placental and fetal growth restriction and abnormalities in heart and lung development, which are also characteristic of the CITED deficient mouse model. However, other features of the mouse Cited2 null phenotype, including exencephaly, adrenal gland agenesis, and prenatal lethality were not associated with CITED2 deficiency in the rat. Trophoblast-specific lentiviral CITED2 knockdown in the rat yielded a growth arrested placental phenotype. Smaller Cited2 null placentas were associated with a growth restricted junctional zone and coincided with a delay in intrauterine trophoblast cell invasion. Invasive trophoblast cells arise from the junctional zone. Transcriptomes of the junctional zone, the invasive trophoblast cell lineage, and differentiating trophoblast stem cells were affected by CITED2 disruption, as were placental adaptations to hypoxia and exposure to viral mimetics. Evidence for the conservation of CITED2 expression in human placental tissue and conserved actions in invasive/extravillous trophoblast cell development were demonstrated. We conclude that CITED2 is a conserved regulator of deep hemochorial placentation.
2023-05-18 | GSE202336 | GEO