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Updated: Jan 30, 2026

Isolation of Human Umbilical Vein Endothelial Cells and Their Use in the Study of Neutrophil Transmigration Under Flow Conditions
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Quantification of adherens junction disruption and contiguous paracellular protein leak in human lung endothelial

Lefeng Wang1,2,3, Justin Chung4, Sean E Gill1,2,3,4

  • 1Centre for Critical Illness Research, Lawson Health Research Institute, London, ON, Canada.

Microcirculation (New York, N.Y. : 1994)
|January 13, 2019
PubMed
Abstract

Insights

Sepsis disrupts VE-cadherin in lung microvascular cells, increasing leakiness. This study links specific VE-cadherin damage to increased paracellular permeability in sepsis, clarifying barrier dysfunction mechanisms.

Area of Science:

  • Cell Biology
  • Pathophysiology
  • Microvascular Endothelial Cells

Background:

  • Sepsis causes microvascular endothelial cell (MVEC) dysfunction, leading to organ edema and inflammation.
  • VE-cadherin, crucial for MVEC adherens junctions, may be disrupted during sepsis.
  • The direct link between individual VE-cadherin disruption and increased paracellular permeability in sepsis remains unclear.

Purpose of the Study:

  • To investigate the mechanistic link between VE-cadherin disruption in human pulmonary MVECs and increased paracellular permeability during sepsis.
  • To assess the correlation between focal VE-cadherin discontinuity and MVEC barrier dysfunction.
  • To provide a basis for detailed assessment of septic MVEC barrier dysfunction mechanisms.

Main Methods:

  • Human pulmonary MVECs were cultured and treated with cytomix (sepsis model) or PBS.
  • MVEC permeability was measured by tracking Oregon green 488-conjugated avidin leak across monolayers.
  • Paracellular leak was correlated with VE-cadherin continuity on individual MVEC surfaces using fluorescence microscopy.

Main Results:

  • Cytomix treatment reduced VE-cadherin density and disrupted its surface continuity, causing intercellular gaps and increased avidin leak.
  • Cytomix-induced MVEC paracellular leak strongly correlated with focal VE-cadherin disruption.
  • Total VE-cadherin density showed a weaker correlation with paracellular leak compared to focal discontinuity.

Conclusions:

  • Septic disruption of VE-cadherin in human lung MVECs is mechanistically linked to contiguous paracellular protein leak.
  • These findings support a direct role for VE-cadherin discontinuity in MVEC barrier dysfunction during sepsis.
  • The study enables more detailed assessment of cell-specific mechanisms underlying septic MVEC barrier dysfunction.
Keywords:
adherens junctionbarrier dysfunctionendothelial cellpermeabilitysepsis

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