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Imaging Leukocyte Adhesion to the Vascular Endothelium at High Intraluminal Pressure
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Pressure is proinflammatory in lung venular capillaries.

W M Kuebler1, X Ying, B Singh

  • 1Department of Medicine, College of Physicians and Surgeons, Columbia University, St. Luke's-Roosevelt Hospital Center, New York, New York 10019, USA.

The Journal of Clinical Investigation
|August 17, 1999
PubMed
Summary

High vascular pressure triggers endothelial calcium influx and fusion pore formation, contributing to inflammation and lung disease. This study reveals a novel mechanism in endothelial cell responses to pressure.

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Area of Science:

  • Cardiovascular biology
  • Cellular physiology
  • Pulmonary medicine

Background:

  • Endothelial cells play a crucial role in vascular health and disease.
  • High vascular pressure is implicated in the pathology of various lung diseases.
  • The precise mechanisms of endothelial response to elevated pressure are not fully understood.

Purpose of the Study:

  • To investigate endothelial responses to high vascular pressure in lung capillaries.
  • To elucidate the role of calcium signaling and exocytosis in these responses.
  • To identify potential therapeutic targets for pressure-induced lung diseases.

Main Methods:

  • Utilized the fura-2 ratioing method to measure intracellular calcium ([Ca(2+)](i)) in endothelial cells.
  • Quantified fusion pore formation using FM1-43 fluorescence.
  • Investigated the effect of blocking mechanogated calcium channels on endothelial responses.

Main Results:

  • Elevated vascular pressure significantly increased endothelial [Ca(2+)](i).
  • Observed a unique spatial-temporal pattern of fusion pore formation, primarily at vascular branch points.
  • Fusion pore formation colocalized with P-selectin expression.
  • Blocking mechanogated calcium channels abolished these pressure-induced endothelial responses.
  • Identified external calcium influx as the critical trigger for these events.

Conclusions:

  • High vascular pressure induces a proinflammatory response in endothelial cells via calcium influx and exocytosis.
  • These findings highlight a novel mechanism contributing to the pathogenesis of pressure-induced lung disease.
  • Targeting mechanogated calcium channels may offer a therapeutic strategy for managing such conditions.