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High-density lipoproteins (HDL) composition and function in preeclampsia.

Yael Einbinder1,2, Tal Biron-Shental2,3, Moran Agassi-Zaitler3

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Summary

Women with preeclampsia (PE) have impaired high-density lipoprotein (HDL) function, with lower paraoxonase1 (PON1) activity and altered apolipoprotein A-1 (ApoA1) release. These HDL changes may increase long-term cardiovascular disease risk in PE patients.

Keywords:
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Area of Science:

  • Cardiovascular Disease
  • Obstetrics
  • Lipid Metabolism

Background:

  • Preeclampsia (PE) is a pregnancy disorder linked to increased future cardiovascular disease (CVD) risk.
  • High-density lipoprotein (HDL) cholesterol, including apolipoprotein A-1 (ApoA1) and paraoxonase1 (PON1), is a known negative predictor of CVD.
  • The inverse relationship between HDL levels and atherosclerotic CVD risk is well-established.

Purpose of the Study:

  • To evaluate the properties of HDL, specifically ApoA1 and PON1, in women with preeclampsia (PE).
  • To assess HDL function in women with PE.
  • To investigate the potential contribution of altered HDL to the increased long-term CVD risk observed in women with PE.

Main Methods:

  • Recruited 25 pregnant women (19 with PE, 6 with normal pregnancy [NP]) at delivery.
  • Isolated HDL from blood samples and analyzed PON1 activity.
  • Utilized an in vitro endothelial cell model to assess HDL's effect on vascular cell adhesion molecule-1 (VCAM-1) and endothelial nitric oxide synthase (eNOS) mRNA expression.

Main Results:

  • Lower PON1 activity was observed in the PE group compared to the NP group (6.51 ± 0.73 vs. 9.98 ± 0.54 units/ml serum; P = 0.015).
  • Increased ApoA1 release from PE-HDL compared to NP-HDL (3.54 ± 0.72 vs. 0.89 ± 0.35; P = 0.01).
  • PE-HDL exposure resulted in increased VCAM-1 and decreased eNOS mRNA expression in TNF-α stimulated endothelial cells compared to NP-HDL.

Conclusions:

  • HDL from women with PE exhibits reduced PON1 activity and increased ApoA1 release, suggesting impaired antioxidant capacity and potential dysfunction.
  • These alterations in HDL properties and function in PE may contribute to the elevated long-term cardiovascular risk associated with the condition.
  • Further research is warranted to elucidate the precise mechanisms linking PE-related HDL changes to future CVD.