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Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption
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Published on: October 4, 2019

Long-term cyclic strain downregulates endothelial Nox4.

Claudia Goettsch1, Winfried Goettsch, Alexander Arsov

  • 1Division of Vascular Endothelium and Microcirculation, Department of Medicine III, University of Technology Dresden, D-01307 Dresden, Germany.

Antioxidants & Redox Signaling
|March 25, 2009
PubMed
Summary

Physiological cyclic strain reduces reactive oxygen species (ROS) by downregulating Nox4 expression in endothelial cells. This mechanism promotes a vasoprotective balance between nitric oxide (NO) and superoxide anions.

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Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanotransduction
  • Oxidative Stress

Background:

  • Endothelial cells experience mechanical forces like cyclic strain in vivo.
  • Nox4-based NAD(P)H oxidase complexes are key sources of superoxide anion (.O(2)(-)) in endothelial cells.

Purpose of the Study:

  • To investigate the impact of cyclic strain on reactive oxygen species (ROS) and nitric oxide (NO) formation in endothelial cells.
  • To elucidate the role of Nox4 in mediating the cellular response to mechanical forces.

Main Methods:

  • Primary human umbilical vein endothelial cells were subjected to cyclic strain (2-18%) for up to 24 hours.
  • ROS formation was measured using electron paramagnetic resonance spectroscopy, cytochrome c assay, and dihydroethidium fluorescence.
  • Gene expression, NO formation, and eNOS activity were assessed via RT-PCR, Western blot, and Griess reaction.

Main Results:

  • Chronic cyclic strain (5-12%) led to a time-dependent downregulation of Nox4 expression and ROS production.
  • Endothelial nitric oxide (NO) formation and endothelial nitric oxide synthase (eNOS) expression were increased by cyclic strain.
  • Strain-induced Nox4 downregulation was inhibited by L-NAME, indicating a role for eNOS.

Conclusions:

  • Physiological cyclic strain downregulates Nox4 expression and reduces superoxide anion formation in endothelial cells.
  • This downregulation is linked to increased NO formation, suggesting a vasoprotective effect.
  • The findings reveal a novel mechanism for maintaining vascular homeostasis under mechanical stress.