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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00018-019-03104-6.

Title:
Human placenta and trophoblast development: key molecular mechanisms and model systems | Cellular and Molecular Life Sciences
Description:
Abnormal placentation is considered as an underlying cause of various pregnancy complications such as miscarriage, preeclampsia and intrauterine growth restriction, the latter increasing the risk for the development of severe disorders in later life such as cardiovascular disease and type 2 diabetes. Despite their importance, the molecular mechanisms governing human placental formation and trophoblast cell lineage specification and differentiation have been poorly unravelled, mostly due to the lack of appropriate cellular model systems. However, over the past few years major progress has been made by establishing self-renewing human trophoblast stem cells and 3-dimensional organoids from human blastocysts and early placental tissues opening the path for detailed molecular investigations. Herein, we summarize the present knowledge about human placental development, its stem cells, progenitors and differentiated cell types in the trophoblast epithelium and the villous core. Anatomy of the early placenta, current model systems, and critical key regulatory factors and signalling cascades governing placentation will be elucidated. In this context, we will discuss the role of the developmental pathways Wingless and Notch, controlling trophoblast stemness/differentiation and formation of invasive trophoblast progenitors, respectively.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Non-Profit & Charity

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Link.springer.com Make Money? {💸}

We're unsure how the site profits.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

pubmed, google, scholar, human, article, cas, trophoblast, cell, cells, placental, placenta, differentiation, development, central, stem, evt, pregnancy, early, expression, villi, maternal, trimester, formation, transcription, role, embryonic, evts, factors, trophoblasts, factor, key, mouse, markers, lineage, tsc, placentation, growth, tscs, model, vitro, knöfler, signalling, uterine, invasion, stb, critical, fetal, gene, fig, extravillous,

Topics {✒️}

fetal hypothalamic-pituitary-adrenal axes hypoxia-inducible factor-dependent manner single-cell rna-seq reveals alpha-t-catenin upregulation article download pdf notch1-negative transient-amplifying cells tcf t-cell factor β-catenin–tcf4 complexes arise wnt/beta-catenin signaling γ-secretase-mediated cleavage gamage & joanna james mesenchymal stem/stromal cells transcription factor tcfap2c/tfap2c htr8/svneo cell line htr-8/svneo cell line transforming growth factor-β single-cell rna-seq rate-limiting vessels regulating homogenous bi-potential population unusual spindle-shaped morphology tcf4–β-catenin complexes meso-endothelial bipotent progenitors syncytin-mediated trophoblastic fusion trophoblast-specific transcription factors macrophage/monocytic markers cd115 extra-embryonic expression pattern activin/nodal pathway inhibition human chorionic gonadotrophin human hand1 gene/cdna growth factor-reduced matrigel uterine natural killer single-cell transcriptomics tcf-negative evt-progenitors human trophoblast side-population progenitor-specific gene myc evt-specific gene expression cd144-positive cells akin evt progenitor-specific genes tgf-beta1-induced differentiation controlling trophoblast stemness/differentiation ctb/te-specific genes key transcription factor reveal distinct populations inhibiting activin/nodal jana lim yt red blood cells developmental pathways wingless nuclear wnt-dependent remain largely elusive early maternal-fetal interface

Questions {❓}

  • A strategy for successful endovascular invasion?
  • Boss AL, Chamley LW, James JL (2018) Placental formation in early pregnancy: how is the centre of the placenta made?
  • Burton GJ, Jauniaux E (2018) Development of the human placenta and fetal heart: synergic or independent?
  • Fisher SJ (2015) Why is placentation abnormal in preeclampsia?
  • Lee CQ et al (2016) What is trophoblast?
  • Part I: What do we know about formative placental development following implantation?
  • Pollheimer J, Fock V, Knöfler M (2014) Review: the ADAM metalloproteinases—novel regulators of trophoblast invasion?
  • Roberts RM et al (2014) Differentiation of trophoblast cells from human embryonic stem cells: to be or not to be?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Human placenta and trophoblast development: key molecular mechanisms and model systems
         description:Abnormal placentation is considered as an underlying cause of various pregnancy complications such as miscarriage, preeclampsia and intrauterine growth restriction, the latter increasing the risk for the development of severe disorders in later life such as cardiovascular disease and type 2 diabetes. Despite their importance, the molecular mechanisms governing human placental formation and trophoblast cell lineage specification and differentiation have been poorly unravelled, mostly due to the lack of appropriate cellular model systems. However, over the past few years major progress has been made by establishing self-renewing human trophoblast stem cells and 3-dimensional organoids from human blastocysts and early placental tissues opening the path for detailed molecular investigations. Herein, we summarize the present knowledge about human placental development, its stem cells, progenitors and differentiated cell types in the trophoblast epithelium and the villous core. Anatomy of the early placenta, current model systems, and critical key regulatory factors and signalling cascades governing placentation will be elucidated. In this context, we will discuss the role of the developmental pathways Wingless and Notch, controlling trophoblast stemness/differentiation and formation of invasive trophoblast progenitors, respectively.
         datePublished:2019-05-03T00:00:00Z
         dateModified:2019-05-03T00:00:00Z
         pageStart:3479
         pageEnd:3496
         license:http://creativecommons.org/licenses/by/4.0/
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         keywords:
            Placenta development
            Chorionic villus
            Trophoblast stem cell
            Trophoblast differentiation
            Mesenchymal cell
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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ScholarlyArticle:
      headline:Human placenta and trophoblast development: key molecular mechanisms and model systems
      description:Abnormal placentation is considered as an underlying cause of various pregnancy complications such as miscarriage, preeclampsia and intrauterine growth restriction, the latter increasing the risk for the development of severe disorders in later life such as cardiovascular disease and type 2 diabetes. Despite their importance, the molecular mechanisms governing human placental formation and trophoblast cell lineage specification and differentiation have been poorly unravelled, mostly due to the lack of appropriate cellular model systems. However, over the past few years major progress has been made by establishing self-renewing human trophoblast stem cells and 3-dimensional organoids from human blastocysts and early placental tissues opening the path for detailed molecular investigations. Herein, we summarize the present knowledge about human placental development, its stem cells, progenitors and differentiated cell types in the trophoblast epithelium and the villous core. Anatomy of the early placenta, current model systems, and critical key regulatory factors and signalling cascades governing placentation will be elucidated. In this context, we will discuss the role of the developmental pathways Wingless and Notch, controlling trophoblast stemness/differentiation and formation of invasive trophoblast progenitors, respectively.
      datePublished:2019-05-03T00:00:00Z
      dateModified:2019-05-03T00:00:00Z
      pageStart:3479
      pageEnd:3496
      license:http://creativecommons.org/licenses/by/4.0/
      sameAs:https://doi.org/10.1007/s00018-019-03104-6
      keywords:
         Placenta development
         Chorionic villus
         Trophoblast stem cell
         Trophoblast differentiation
         Mesenchymal cell
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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                  name:Medical University of Vienna
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                     name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
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               name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
               type:PostalAddress
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      email:[email protected]
      name:Sandra Haider
      affiliation:
            name:Medical University of Vienna
            address:
               name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
               type:PostalAddress
            type:Organization
      name:Leila Saleh
      affiliation:
            name:Medical University of Vienna
            address:
               name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
               type:PostalAddress
            type:Organization
      name:Jürgen Pollheimer
      affiliation:
            name:Medical University of Vienna
            address:
               name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
               type:PostalAddress
            type:Organization
      name:Teena K. J. B. Gamage
      affiliation:
            name:University of Auckland
            address:
               name:Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
               type:PostalAddress
            type:Organization
      name:Joanna James
      affiliation:
            name:University of Auckland
            address:
               name:Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
      name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
      name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
      name:Reproductive Biology Unit, Department of Obstetrics and Gynaecology, Medical University of Vienna, Vienna, Austria
      name:Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
      name:Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand

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