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Nicotinamide Riboside Mitigates Antiphospholipid Antibody-Induced Dysfunction in Human Trophoblast Cells.

Abigail C Fischer1, Hanah M Georges1, Deidre M Jones2

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American Journal of Reproductive Immunology (New York, N.Y. : 1989)
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Nicotinamide riboside (NR) reduced inflammation and oxidative stress in trophoblast cells exposed to antiphospholipid antibodies (aPL). However, NR did not improve aPL-induced trophoblast cell migration, suggesting partial benefits for obstetric antiphospholipid syndrome.

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Area of Science:

  • Obstetrics and Gynecology
  • Immunology
  • Cell Biology

Background:

  • Obstetric antiphospholipid syndrome (APS) involves anti-phospholipid antibodies (aPL) disrupting placentation, leading to adverse pregnancy outcomes like fetal loss and preterm birth.
  • aPL targeting beta 2 glycoprotein 1 (β2GPI) induce trophoblast inflammation, oxidative stress, and impaired angiogenic factor production, contributing to pregnancy complications.
  • The antioxidant nicotinamide riboside (NR) is investigated for its potential to counteract these detrimental effects.

Purpose of the Study:

  • To determine if the antioxidant nicotinamide riboside (NR) can mitigate the adverse effects of anti-phospholipid antibodies (aPL) on human trophoblast cells.
  • To investigate the impact of NR on aPL-induced inflammation, oxidative stress, angiogenic factor production, and cell migration in trophoblast cells.

Main Methods:

  • Human first-trimester trophoblast cells (Sw.71) were treated with aPL in the presence or absence of NR.
  • Pro-inflammatory cytokines, chemokines, and angiogenic factors in trophoblast supernatants were quantified using ELISA.
  • Reactive oxygen species (ROS) production and cell migration were assessed using fluorescence and colorimetric assays, respectively.

Main Results:

  • Nicotinamide riboside (NR) effectively blocked aPL-induced inflammation and reactive oxygen species (ROS) production in trophoblast cells.
  • NR reversed the negative impact of aPL on the production of angiogenic factors by trophoblast cells.
  • NR did not rescue the impaired migratory capacity of trophoblast cells induced by aPL.

Conclusions:

  • Nicotinamide riboside (NR) demonstrates a partial protective effect against aPL-induced trophoblast dysfunction, specifically mitigating inflammation and oxidative stress.
  • The inability of NR to restore trophoblast cell migration highlights the complexity of aPL-mediated damage in obstetric APS.
  • These findings suggest antioxidant therapies like NR warrant further investigation as a potential management strategy for obstetric antiphospholipid syndrome.