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Molecular pathways of senescence regulate placental structure and function.

Hilah Gal1, Marina Lysenko2, Sima Stroganov1

  • 1Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.

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|August 20, 2019
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Summary

Cellular senescence in the placenta is crucial for fetal development. Reduced senescence markers in intrauterine growth restriction pregnancies suggest impaired placental function, impacting fetal nourishment.

Keywords:
gelatinaseintrauterine growth restrictionplacentasenescencesyncytiotrophoblast

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Area of Science:

  • Reproductive biology
  • Cellular senescence
  • Placental development

Background:

  • The placenta's syncytiotrophoblast layer, vital for fetal nourishment, displays cellular senescence characteristics.
  • Reduced senescence markers are observed in human placentas from pregnancies with intrauterine growth restriction (IUGR).

Purpose of the Study:

  • To investigate the role of senescence pathways in syncytiotrophoblast function.
  • To understand how attenuated senescence affects placental structure and dynamics.

Main Methods:

  • Utilized dynamic contrast-enhanced MRI in mouse models with altered senescence programs (p53-/-, Cdkn2a-/-, and Cdkn2a-/-;p53-/-).
  • Analyzed human primary syncytiotrophoblast for senescence markers and associated molecular pathways.
  • Examined placental histopathology in mouse models.

Main Results:

  • Dynamic contrast-enhanced MRI revealed altered placental dynamics in mice with attenuated senescence.
  • Histopathological changes were observed in the placental labyrinths of these mice.
  • Human syncytiotrophoblast upregulated senescence markers, cell-cycle inhibition, and senescence-associated secretory phenotype (SASP) pathways.
  • SASP pathways were compromised in placentas with attenuated senescence and in human IUGR pregnancies.

Conclusions:

  • Molecular mediators of senescence are critical regulators of placental structure and function.
  • Senescence influences placental development through both cell-autonomous and non-autonomous mechanisms.
  • Impaired senescence pathways may contribute to placental dysfunction in IUGR.