• Anesthesia and analgesia · Apr 2022

    Extracellular Vesicles From Women With Severe Preeclampsia Impair Vascular Endothelial Function.

    • Saravanakumar Murugesan, Hanna Hussey, Lakshmi Saravanakumar, Rachel G Sinkey, Adam B Sturdivant, Mark F Powell, and Dan E Berkowitz.
    • From the Department of Anesthesiology and Perioperative Medicine, Division of Molecular and Translational Biomedicine.
    • Anesth. Analg. 2022 Apr 1; 134 (4): 713-723.

    BackgroundPreeclampsia (PE) manifesting as hypertension and organ injury is mediated by vascular dysfunction. In biological fluids, extracellular vesicles (EVs) containing microRNA (miRNA), protein, and other cargo released from the placenta may serve as carriers to propagate injury, altering the functional phenotype of endothelial cells. PE has been consistently correlated with increased levels of placenta-derived EVs (pEVs) in maternal circulation. However, whether pEVs impaired endothelial cell function remains to be determined. In this study, we hypothesize that pEVs from pregnant women with severe PE (sPE) impair endothelial function through altered cell signaling.MethodsWe obtained plasma samples from women with sPE (n = 14) and normotensive pregnant women (n = 15) for the isolation of EVs. The total number of EV and pEV contribution was determined by quantifying immunoreactive EV-cluster of designation 63 (CD63) and placental alkaline phosphatase (PLAP) as placenta-specific markers, respectively. Vascular endothelial functional assays were determined by cell migration, electric cell-substrate impedance sensing in human aortic endothelial cells (HAECs), and wire myography in isolated blood vessels, preincubated with EVs from normotensive and sPE women.ResultsPlasma EV and pEV levels were increased in sPE when compared to normotensive without a significant size distribution difference in sPE (108.8 ± 30.2 nm) and normotensive-EVs (101.3 ± 20.3 nm). Impaired endothelial repair and proliferation, reduced endothelial barrier function, reduced endothelial-dependent vasorelaxation, and decreased nitrite level indicate that sPE-EVs induced vascular endothelial dysfunction. Moreover, sPE-EVs significantly downregulated endothelial nitric oxide synthase (eNOS and p-eNOS) when compared to normotensive-EV.ConclusionsEVs from sPE women impair endothelial-dependent vascular functions in vitro.Copyright © 2021 International Anesthesia Research Society.

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