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Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
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Bradykinin does not induce gap formation between human endothelial cells.

Pia Jungmann1, Marianne Wilhelmi, Hans Oberleithner

  • 1Institute of Physiology II, University of Münster, Robert-Koch-Str. 27b, 48149 Münster, Germany.

Pflugers Archiv : European Journal of Physiology
|October 3, 2007
PubMed
Summary

Bradykinin increases endothelial permeability via transcellular fluid passage, not paracellular gaps. This study used atomic force microscopy and permeability assays to differentiate fluid transport mechanisms in endothelial cells.

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Area of Science:

  • Cell Biology
  • Physiology
  • Biophysics

Background:

  • Endothelial permeability is crucial for vascular fluid balance and inflammation.
  • Paracellular gaps are traditionally considered the primary route for fluid transport across endothelia.
  • Bradykinin's precise mechanism for increasing endothelial permeability remains unclear.

Purpose of the Study:

  • To investigate whether bradykinin increases endothelial permeability through paracellular gap formation or transcellular fluid passage.
  • To differentiate between paracellular and transcellular routes of fluid transport.
  • To elucidate the cellular mechanisms underlying bradykinin-induced permeability changes.

Main Methods:

  • Human umbilical vein endothelial cells were analyzed using atomic force microscopy (AFM) to visualize cellular junctions.
  • A modified permeability assay with a rapid cooling protocol was employed to distinguish vesicular (transcellular) from non-vesicular (paracellular) transport.
  • Fluorescence microscopy was used to quantify endocytotic vesicle formation.

Main Results:

  • Bradykinin (1 microM) did not induce significant alterations at cellular junctions, as observed by AFM.
  • Bradykinin enhanced fluorescein isothiocyanate-dextran permeability by 48%, which was blocked by rapid cooling, indicating a vesicular mechanism.
  • Ionomycin (1 microM) induced significant paracellular gap formation, confirmed by persistent permeability after cooling.
  • Bradykinin upregulated endocytotic vesicle formation by 68%, while ionomycin had no significant effect.

Conclusions:

  • Bradykinin promotes transcellular fluid passage through vesicular transport.
  • The findings challenge the notion that paracellular gap formation is the sole mechanism for bradykinin-induced permeability increase.
  • Bradykinin's effects on endothelial permeability are primarily mediated by transcellular routes, distinct from ionomycin-induced paracellular leakage.