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Association between atherogenic risk-modulating proteins and endothelium-dependent flow-mediated dilation in coronary

Andrea Tryfonos1,2, Joseph Mills3, Daniel J Green4

  • 1Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, L3 3AF, UK.

European Journal of Applied Physiology
|October 28, 2022
PubMed

Insights

Endothelial dysfunction in coronary artery disease (CAD) patients is linked to specific protein expressions. eNOS Ser1177 phosphorylation may be key in maintaining vasodilation in CAD.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Function
  • Atherosclerosis Research

Background:

  • Endothelial dysfunction is a primary factor in atherosclerosis and coronary artery disease (CAD).
  • Key implicated pathways include reduced nitric oxide (NO) bioavailability, oxidative stress, vasoconstriction, inflammation, and senescence.
  • Limited data exist on the direct in vivo associations between these pathways and endothelial function measures in CAD patients.

Purpose of the Study:

  • To investigate the relationships between in vivo vascular function measurements and the expression of atherogenic risk-modulating proteins in endothelial cells (ECs) from CAD patients.
  • To explore the role of specific proteins, including eNOS, NOX2, NFκB, ET-1, and senescence markers (p53, p21, p16), in endothelial dysfunction within the context of CAD.

Main Methods:

  • Vascular function was assessed in 56 CAD patients using flow-mediated dilation (FMD) and exercise-induced handgrip hyperemia (HE%) via trans-radial catheterization.
  • Endothelial cells (ECs) were isolated from the radial artery during catheterization.
  • Protein levels of eNOS, NOX2, NFκB, ET-1, senescence markers (p53, p21, p16), nitrotyrosine, and eNOS Ser1177 phosphorylation were quantified.

Main Results:

  • Flow-mediated dilation (FMD) showed positive associations with eNOS Ser1177 phosphorylation (r=0.290, P=0.037), and protein levels of p21 (r=0.307, P=0.027) and p16 (r=0.426, P=0.002).
  • No significant associations were found between FMD and markers of oxidative stress, vasoconstriction, or inflammation.
  • Exercise-induced hyperemia (HE%) did not correlate with any measured EC proteins.

Conclusions:

  • The study highlights differences in endothelium-dependent vasodilation regulation in CAD patients compared to healthy individuals.
  • eNOS Ser1177 phosphorylation appears to be a critical factor in maintaining vasodilation in CAD patients.
  • These findings suggest specific molecular mechanisms underlying endothelial dysfunction in CAD.
Abstract

Keywords:
AtherosclerosisCoronary artery diseaseEndothelial cellsEndothelial dysfunctionExercise-induced dilationFlow-mediated dilation

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