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Force Chains And Gap Formation in Thrombin‐induced Endothelial Permeability
Author(s) -
Krishnan Ramaswamy,
Hardin Corey,
Dang Quynh,
Manomohan Greeshma,
Tian Xinyong,
Dubrovski Oleksii,
Tambe Dhananjay,
Jader Colombo,
Gado Emanuela,
Butler James,
Fredberg Jeffrey,
Birukov Konstantin
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.85.5
Subject(s) - monolayer , biophysics , intracellular , paracellular transport , chemistry , gap junction , permeability (electromagnetism) , endothelial stem cell , ve cadherin , cell junction , transcellular , thrombin , cell , materials science , microbiology and biotechnology , cadherin , membrane , biology , biochemistry , immunology , in vitro , platelet
Methods: Cell‐substrate forces and intercellular stresses were measured in cultured human pulmonary artery endothelial cells using Fourier Transform Traction Microscopy and Monolayer Stress Microscopy, respectively. Thrombin (0.3U/ml) induced paracellular gaps were visualized using XPeRT. Results: In untreated monolayers, intercellular stresses were spatially heterogeneous, highly cooperative over approximately 10 cell diameters and aligned into extended force chains. When the monolayers were perturbed by thrombin, gap formation was seen to be similarly cooperative and associated with enlargement of force chains far outside the gap region. Disruption of the cell‐cell junction by knockdown of VE‐cadherin resulted not only in an overall decrease in levels of intercellular stress but also their spatial correlation. Discussion Gap formation and underlying VE‐cadherin‐mediated redistribution of mechanical stresses within the monolayer are non‐local, highly cooperative and reminiscent of dynamic stresses and structural rearrangements observed within jammed granular materials.