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Softening of hyperoxia treated alveolar epithelial cells reduces stretch‐induced injury
Author(s) -
Wilhelm Kristina Rebecca,
Roan Esra,
Gosh Maik,
Waters Christopher M.
Publication year - 2013
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.27.1_supplement.914.11
Subject(s) - hyperoxia , ards , mechanical ventilation , contractility , softening , chemistry , medicine , microbiology and biotechnology , lung , anesthesia , materials science , biology , composite material
Objectives Acute respiratory distress syndrome (ARDS) patients are administered high concentrations of oxygen during mechanical ventilation; hyperoxia and mechanical ventilation can independently cause injury. The combination may even accelerate the injury, but how this injury occurs is still not fully understood. Here we show that stretch‐induced injury following hyperoxia is a function of cell elasticity (E). Methods We utilized an atomic force microscope (Asylum) in the indentation‐mode to measure E in cultured alveolar epithelial cells, and a cell‐stretch device to mimic mechanical ventilation. Cell detachment was determined following pre‐treatment with hyperoxia and subsequent cell stretching. Results Hyperoxia increased cell elasticity of lung epithelial cells, thus making them more brittle and more susceptible to stretch‐induced injury (Roan et. al). Decreasing E (softening) the cells after hyperoxia treatment by inhibiting RhoA Kinase (Y‐27632), by decreasing f‐actin (cytochalasin D), or by reducing acto‐myosin contractility (blebbistatin) reduced subsequent stretched‐induced injury. Conclusion Stretch‐induced injury in ARDS patients may be reduced by lowering the stiffness of cells.