Christopher M. Waters, Ph.D.

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Professor and Interim Chair
71 S. Manassas St.
Translational Research Building
Memphis, TN 38163
Phone: 901-448-5799


B.S.E., Chemical Engineering, University of Tennessee at Chattanooga, 1985
M.S., Biomedical Engineering, University of Miami, FL, 1987
Ph.D., Biomedical Engineering, Vanderbilt University, 1991
Post Doc, Biomedical Engineering, Vanderbilt University, 1991-1992


Research Interests

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My laboratory focuses on mechanobiology and acute lung injury. Acute respiratory distress syndrome is a severe form of acute lung injury that can develop from pneumonia, influenza, sepsis, trauma, smoke inhalation, and other causes. Patients with 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. Clinical trials have demonstrated a substantial reduction in mortality in ARDS patients when ventilation strategies are used that reduce overdistention (lower tidal volumes) and minimize airway collapse and reopening (positive end expiratory pressure). 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.  In addition, the use of supplemental oxygen (hyperoxia) in ARDS patients can exacerbate mechanically induced injury.

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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 signaling pathways involved in the development of lung injury such as the stimulation of reactive oxygen species, the regulation of MAP kinases by apoptosis signal regulating kinase (ASK1), how changes in mechanical properties of cells contributes to injury, and the activation of inflammatory pathways including the inflammasome.  We also study mechanisms of epithelial repair including cell migration and wound healing, chemokine signaling involving the CXCL12/CXCR4 pathway, Rho GTPase signaling, cytoskeletal remodeling, and regional variations in cellular tension. My 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.

Representative Publications

  • Wilhelm, K., E. Roan, A. Bada, and C.M. Waters.  Kymographic imaging of the elastic modulus of epithelial cells during onset of migration, Biophys. J. 109 (10):  2051-2057, 2015.  PMCID:  PMC4656878.
  • Rapalo, G., J.D. Herwig, R. Hewitt, K. Wilhelm, C.M. Waters, and E. Roan.  Live cell imaging during mechanical stretch, J. Vis. Exp (JoVE) (102):  e52737, 2015.  PMCID:  PMC4692539.
  • Schwingshackl, A., B. Teng, P. Makena, M. Ghosh, S.E. Sinclair, C. Luellen, L. Balasz, C. Rovnaghi, R.M. Bryan, E. Lloyd, E. Fitzpatrick, J.S. Saravia, S. Cormier, and C.M. Waters.  Deficiency of the two-pore potassium (K2P) channel Trek-1 promotes hyperoxia-induced lung injury, Crit. Care Med. 42(11):  e692-e701, 2014.  PMCID:  PMC4199872
  • Wilhelm, K., E. Roan, M. Ghosh, K. Parthasarathi, and C.M. Waters.  Hyperoxia increases the elastic modulus of alveolar epithelial cells through Rho kinase, FEBS J. 281:  957-969, 2014.  PMCID:  PMC3916181
  • Ghosh, M.C., V. Gorantla, P.S. Makena, C. Luellen, S.E. Sinclair, and C.M. Waters.  Insulin like growth factor-1 stimulates differentiation of ATII cells to ATI-like cells through activation of Wnt5a, Am. J. Physiol. Lung Cell. Mol. Physiol. 305:  L222-L228, 2013.  PMCID:  PMC3743013
  • Ghosh, M.C., P.S. Makena, V. Gorantla, S.E. Sinclair, and C.M. Waters.  CXCR4 regulates migration of lung alveolar epithelial cells through activation of Rac1 and matrix metalloproteinase-2 (MMP-2), Am. J. Physiol. Lung Cell. Mol. Physiol. 302:  L846-L856, 2012.  PMCID:  PMC3362158
  • Makena, P.S., V.K. Gorantla, M.C. Ghosh, L. Bezawada, K. Kandasamy, L. Balazs, C. Luellen, K.E. Thompson, K. Parthasarathi, H. Ichijo, C.M. Waters, and S.E. Sinclair.  Deletion of apoptosis signal regulating kinase-1 prevents ventilator-induced lung injury in mice, Am. J. Resp. Cell Mol. Biol. 46:  461-469, 2012.  PMCID:  PMC3359950

Additional Information