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PPARgamma and early human placental development.

Thierry Fournier1, Patrice Thérond, Karen Handschuh

  • 1INSERM, U767, Faculté des Sciences Pharmaceutiques et Biologiques, 4 avenue de l'Observatoire, 75006 Paris, France. Thierry.Fournier@univ-paris5.fr

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Peroxisome proliferator-activated receptor-gamma (PPARgamma) activation inhibits human trophoblast invasion, crucial for placental development and preventing preeclampsia. Oxidized-low-density lipoproteins (ox-LDLs) may modulate this process via PPARgamma and liver X receptor beta (LXRbeta).

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Area of Science:

  • Reproductive Biology and Endocrinology
  • Molecular and Cellular Biology
  • Obstetrics and Gynecology

Background:

  • The placenta is vital for fetal growth and pregnancy outcome, with early development involving extensive trophoblast invasion and uterine remodeling.
  • Abnormal trophoblast invasion is linked to poor placentation, fetal growth defects, and preeclampsia, a major pregnancy complication.
  • Peroxisome proliferator-activated receptor-gamma (PPARgamma) is essential for placental development in mice, but its role in human trophoblast invasion was unclear.

Purpose of the Study:

  • To investigate the role of PPARgamma in controlling human trophoblast invasion during early placental development.
  • To explore the mechanisms underlying PPARgamma-mediated effects on trophoblast invasion.
  • To understand the potential contribution of oxidized-low-density lipoproteins (ox-LDLs) to trophoblast invasion modulation and its relevance to preeclampsia.

Main Methods:

  • Development of in vitro models of human invasive trophoblasts.
  • Treatment with PPARgamma agonists and analysis of trophoblast invasion.
  • Analysis of PPARgamma-target genes and identification of potential ligands like ox-LDLs, eicosanoids, and oxysterols.
  • Investigation of liver X receptor beta (LXRbeta) expression and the effects of LXR agonists on trophoblast invasion.

Main Results:

  • Activation of PPARgamma by agonists significantly inhibited human trophoblast invasion in a concentration-dependent manner.
  • PPARgamma-target genes, including placental growth hormone, PAPP-A, and hCG, may mediate effects in an autocrine fashion.
  • Oxidized-low-density lipoproteins (ox-LDLs), found at the maternofetal interface, contain PPARgamma agonists and inhibit trophoblast invasion.
  • Oxysterols within ox-LDLs activate LXRbeta, another nuclear receptor expressed in trophoblasts, which also inhibits invasion.

Conclusions:

  • PPARgamma plays a critical role in regulating human trophoblast invasion during early placental development.
  • Ligands such as ox-LDLs present at the implantation site can modulate trophoblast invasion through PPARgamma and LXRbeta activation.
  • These findings provide new insights into the mechanisms controlling placental development and offer potential targets for understanding and managing preeclampsia.