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Rho Kinase-Mediated Reduction in Cardiac Capillary Endothelial Cell Dimensions, In Situ, Against Flow

Matthew C Glyn1, John G Lawrenson, Barbara J Ward

  • 1Leukocyte Biology, National Heart and Lung Institute, Sir Alexander Fleming Building, South Kensington Campus, Imperial College London, London, UK. m.glyn@imperial.ac.uk

Microcirculation (New York, N.Y. : 1994)
|May 23, 2008
PubMed

Insights

Histamine reduces cardiac capillary endothelial cell size in rat hearts, even with blood flow. This shape change, mediated by Rho kinase (ROK), mimics ischemia effects and offers potential therapeutic targets.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Physiology
  • Myocardial Ischemia Research

Background:

  • Previous studies demonstrated ischemia reduces cardiac capillary caliber via endothelial cell shrinkage.
  • This shrinkage was linked to Rho kinase (ROK) activity and actin cytoskeleton stabilization.

Purpose of the Study:

  • To investigate if endothelial cell shape changes, similar to those in ischemia, can occur in capillaries with continuous blood flow.
  • To determine the role of Rho kinase (ROK) in mediating these flow-induced changes.

Main Methods:

  • Utilized Langendorff-perfused rat hearts subjected to vasoactive agents, ischemia, and reperfusion.
  • Measured capillary endothelial cell dimensions (perimeters, areas) from electron micrographs.
  • Assessed the effect of Rho kinase (ROK) inhibition on histamine-induced changes.

Main Results:

  • Histamine (100 microM) induced significant reductions in capillary endothelial cell dimensions in situ without causing endothelial injury.
  • These histamine-induced morphometric changes were prevented by Rho kinase (ROK) inhibition.
  • The observed changes mimicked those previously seen following myocardial ischemia.

Conclusions:

  • Cardiac capillary endothelial cells can alter their shape in response to stimuli even under continuous flow.
  • Histamine triggers ROK-dependent endothelial cell shape changes that resemble those induced by ischemia.
  • Targeting the actomyosin contractile system presents a potential strategy to mitigate ischemia-induced myocardial damage.
Abstract

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