Long-range stress transmission guides endothelial gap formation
Autor: | Jeffrey J. Fredberg, Emanuela Del Gado, Dhananjay T. Tambe, Jader Colombo, James P. Butler, C. Corey Hardin, Joyjit Chattoraj, Trong Nguyen, Greeshma Manomohan, Konstantin G. Birukov, Ramaswamy Krishnan |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Materials science Cell Membrane Permeability Endothelial permeability Biophysics Nanotechnology 01 natural sciences Biochemistry Mechanotransduction Cellular Article Stress (mechanics) 03 medical and health sciences 0103 physical sciences Ultimate tensile strength Cell Adhesion Humans Computer Simulation 010306 general physics Molecular Biology Cells Cultured Range (particle radiation) Cell layer Models Cardiovascular Endothelial Cells Gap Junctions Cell Biology 030104 developmental biology Paracellular transport Tension (geology) Stress Mechanical Shear Strength |
Zdroj: | Biochemical and biophysical research communications. 495(1) |
ISSN: | 1090-2104 |
Popis: | In endothelial gap formation, local tractions exerted by the cell upon its basal adhesions are thought to exceed balancing tensile stresses exerted across the cell-cell junction, thus causing the junction to rupture. To test this idea, we mapped evolving tractions, intercellular stresses, and corresponding growth of paracellular gaps in response to agonist challenge. Contrary to expectation, we found little to no relationship between local tensile stresses and gap formation. Instead, we discovered that intercellular stresses were aligned into striking multi-cellular domains punctuated by defects in stress alignment. Surprisingly, gaps emerged preferentially not at stress hotspots, as predicted, but rather at stress defects. This unexpected behavior is captured by a minimal model of the cell layer as a jammed assembly of cohesive particles undergoing plastic rearrangements under tension. Together, experiments and model suggest a new physical picture in which gap formation, and its consequent effect on endothelial permeability, is determined not by a local stress imbalance at a cell-cell junction but rather by emergence of non-local, cooperative stress reorganization across the cellular collective. |
Databáze: | OpenAIRE |
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