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Related Experiment Videos

Shear stress and endothelial cell activation.

Aron B Fisher1, Abu B Al-Mehdi, Yefim Manevich

  • 1Institute for Environmental Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6068, USA.

Critical Care Medicine
|May 11, 2002
PubMed
Summary

Loss of blood flow (ischemia) triggers rapid endothelial cell changes, including membrane depolarization and reactive oxygen species production. These events initiate a signaling pathway potentially aimed at restoring blood flow and forming new capillaries.

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Area of Science:

  • Endothelial cell biology
  • Cardiovascular research
  • Mechanobiology

Background:

  • Ischemia in isolated rat lungs causes lipid and protein oxidation, indicating reactive oxygen species (ROS) generation.
  • Previous work established ROS generation during ischemia in ventilated rat lungs.

Purpose of the Study:

  • To elucidate the initial cellular events and signaling pathways in response to ischemia in endothelial cells.
  • To investigate the role of shear stress and mechanotransduction in endothelial cell responses to ischemia.

Main Methods:

  • Utilized biochemical and imaging techniques in isolated rat lungs and adapted endothelial cells.
  • Employed in vitro models to study endothelial cells adapted to shear stress.
  • Measured membrane potential, NADPH oxidase activity, intracellular calcium (Ca2+), and nitric oxide (NO) generation.

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Main Results:

  • Ischemia rapidly induced endothelial cell plasma membrane depolarization within seconds.
  • Activation of NADPH oxidase led to superoxide anion and hydrogen peroxide (H2O2) generation.
  • Intracellular Ca2+ levels increased, followed by Ca2+ influx and elevated nitric oxide generation.
  • In vitro models showed ROS-dependent activation of NF-κB and AP-1, with increased cell division after 24 hours of ischemia.

Conclusions:

  • Endothelial cell responses to ischemia are primarily driven by altered shear stress (mechanotransduction), not metabolic changes.
  • A novel cell-signaling pathway involving ROS, Ca2+, and NO is activated by loss of shear stress.
  • This response may serve to restore blood flow via vasodilation and promote angiogenesis.