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In Vitro Differentiation of Human Pluripotent Stem Cells into Trophoblastic Cells
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PPARγ and human trophoblast differentiation.

Thierry Fournier1, Jean Guibourdenche, Karen Handschuh

  • 1INSERM, U767, 4 Avenue de l'Observatoire, Paris F-75006, France. Thierry.Fournier@parisdescartes.fr

Journal of Reproductive Immunology
|June 28, 2011
PubMed
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Peroxisome proliferator-activated receptor-γ (PPARγ) plays a crucial role in human placental development by regulating trophoblast differentiation and invasion. Dysregulation of PPARγ, potentially by HCMV infection, can negatively impact implantation and embryonic development.

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Area of Science:

  • Reproductive Biology
  • Molecular Endocrinology
  • Cell Biology

Background:

  • Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear receptor regulating energy homeostasis, cell differentiation, and inflammation.
  • PPARγ is unexpectedly essential for placental development, with specific expression in human trophoblasts.
  • PPARγ activation influences trophoblast lipid accumulation, differentiation, and invasiveness.

Purpose of the Study:

  • To investigate the role of PPARγ and its target genes in human trophoblast differentiation and invasion.
  • To explore the impact of oxidized LDLs and human cytomegalovirus (HCMV) on trophoblastic PPARγ activity.
  • To analyze the differential regulation of hCG by PPARγ in distinct trophoblast subtypes.

Main Methods:

  • In vitro studies using human trophoblast cell lines.
  • Analysis of PPARγ transcriptional activity in response to oxidized LDLs.
  • Investigation of PPARγ target gene expression, including hCG.
  • Examination of hCG regulation in different trophoblast subtypes.

Main Results:

  • Oxidized LDLs activate PPARγ and inhibit trophoblast invasion.
  • HCMV infection activates trophoblastic PPARγ, inhibiting cytotrophoblast invasiveness.
  • PPARγ differentially regulates hCG gene expression in villous and extravillous trophoblasts.
  • A hyperglycosylated hCG form (hCG-H) produced by invasive EVCT promotes trophoblast invasion.

Conclusions:

  • PPARγ and its target genes, like hCG, are critical for human trophoblast differentiation and invasion.
  • Over-activation of PPARγ at the maternal-fetal interface may impair implantation and placentation.
  • HCMV infection-induced PPARγ over-activation could negatively affect embryonic development.