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Effect of Cytoskeletal Structure on Cellular Necrosis during Airway Reopening
Author(s) -
Ghadiali Samir N,
Yalcin Huseyin,
Dailey Hannah
Publication year - 2007
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.21.5.a555-d
Subject(s) - cytoskeleton , actin , microbiology and biotechnology , actin cytoskeleton , cell , necrosis , chemistry , biophysics , motility , programmed cell death , biology , pathology , medicine , apoptosis , biochemistry
The reopening of fluid‐filled airways involves the application of surface tension forces on the airway epithelium. In addition to the magnitude of these forces, the amount of cellular deformation and/or necrosis may also depend on the epithelial cell's microstructural properties. In this study, we utilized an in‐vitro cell culture model of airway reopening to investigate how cytoskeletal properties influence cellular injury. The actin cytoskeleton was altered with various chemical agents (jasplakinolide, latrunculin and histamine) and changes in cytoskeletal structure were monitored with fluorescent microscopy. Standard live/dead staining was used to quantify cell death. Stabilizing the actin cytoskeleton resulted in decreased cell death while treatment with histamine had no effect. Surprisingly, destabilizing the actin cytoskeleton resulted in a significant decrease in cell death. We hypothesize that cells treated with the actin destabilizer behave more like a viscous fluid than an elastic solid. The increased viscoelastic time constant may dampen out the transient hydrodynamic forces exerted during airway reopening. We have used both direct experimental measurements of cell mechanics and computational models cell deformation to further investigate this hypothesis. This work was supported by the American Heart Association and SNG is a Parker B. Francis Fellow of Pulmonary Research.