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Endothelin-1-induced endothelial microvesicles impair endothelial cell function.

L Madden Brewster1, Vinicius P Garcia1, Ma'ayan V Levy1

  • 1Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|April 24, 2020
PubMed
Summary
This summary is machine-generated.

Endothelin-1 (ET-1) triggers the release of endothelial microvesicles (EMVs) that promote inflammation and impair nitric oxide synthase (eNOS) function in endothelial cells. These ET-1-generated EMVs contribute to the pro-atherogenic effects of ET-1.

Keywords:
eNOSendothelial cellsendothelin-1inflammationmicrovesicles

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Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Biology
  • Molecular Medicine

Background:

  • Endothelin-1 (ET-1) is a key regulator of vascular tone, and its overexpression is linked to atherosclerosis.
  • Endothelial microvesicles (EMVs) are released by endothelial cells and play critical roles in vascular health and disease.
  • The functional characteristics of EMVs are influenced by the conditions under which they are released.

Purpose of the Study:

  • To investigate the impact of ET-1-induced EMVs on endothelial cell inflammation, apoptosis, and endothelial nitric oxide synthase (eNOS) activity.
  • To compare the effects of ET-1-generated EMVs with those of ET-1 alone and control EMVs.
  • To elucidate the role of ET-1-generated EMVs in the pro-atherogenic effects of ET-1.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were treated with ET-1 or vehicle.
  • EMVs released from treated HUVECs were isolated and quantified.
  • Fresh HUVECs were exposed to ET-1, ET-1-induced EMVs, or control EMVs, followed by analysis of inflammatory markers (IL-6, IL-8, NF-κB p65), apoptosis markers (caspases), and eNOS expression and activation.

Main Results:

  • ET-1 significantly increased EMV release from HUVECs compared to controls.
  • ET-1-generated EMVs markedly elevated IL-6, IL-8, and NF-κB p65 expression, indicating increased endothelial inflammation.
  • No significant differences in caspase-9 or caspase-3 activation were observed between ET-1-EMV and control EMV treatments.
  • ET-1-generated EMVs significantly reduced total and activated eNOS levels, impairing endothelial nitric oxide production.
  • The effects of ET-1-generated EMVs on endothelial cells were comparable to the direct effects of ET-1.

Conclusions:

  • ET-1 induces a specific phenotype in EMVs that detrimentally affects endothelial cell function.
  • ET-1-generated EMVs contribute to endothelial inflammation and dysfunction by reducing eNOS activity.
  • These findings suggest that ET-1-derived EMVs are key mediators in the pro-atherogenic actions of ET-1.