Cellular Biomechanical Responses

This study area focuses on mechanobiology and acute lung injury. Patients with acute respiratory distress syndrome (ARDS) are placed on mechanical ventilators to improve oxygenation, but the ventilator may cause additional injury to the lungs due to either overdistention or airway collapse and reopening.  The lung is a mechanically dynamic organ, and cells in the lung are subjected to shear stress due to fluid flow, tensile and compressive forces due to respiratory motion, and normal forces due to vascular or airway pressure.  High tidal volume mechanical ventilation in injured lungs induces mechanical stresses that increase injury to the lung epithelium, stimulate inflammatory responses, and decrease repair mechanisms.  We are focusing on the mechanisms by which mechanical forces contribute to lung injury, inhibit wound healing of lung epithelial cells, and stimulate inflammation.  We are examining cell migration and wound healing, Rho GTPase signaling, cytoskeletal remodeling, stimulation of reactive oxygen species, cytokine secretion, and regional variations in cellular tension.  In addition we are examining lung injury in vivo and the effects of exposure to high levels of oxygen (hyperoxia).  The research seeks to identify the levels of mechanical forces and the types of lung injury that cells experience in vivo, to develop in vitro models to evaluate cellular responses, and to identify mechanisms by which mechanical forces are transduced into biological signals.

For additional information you may contact the following faculty:
Chris Waters (UTHSC)
Esra Roan (UoM)

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