Mechanism of Cell Damage in Glaucoma: Effect of Rapid Depressurization on Cells
Matthew Glucksberg, PhD
Northwestern University (Chicago, IL)
July 1, 2013 to December 31, 2014
Grant Reference ID:
Mark Johnson, PhD
Northwestern University (Evanston, IL)
Effect of Rapid Depressurization on Cultured Cells
The importance of controlling pressure in the eye is known to be a factor in the damage to vision caused by glaucoma. The reason why controlling pressure is so important is still not known, but there are several hypotheses involving the stresses and strains caused by elevated pressure in the tissue of the optic nerve. However, in recent years a number of studies have supported an alternate hypothesis that it is not the stresses and strains alone that cause the high pressure, but the high pressure itself does the damage. Drs. Gluckberg and Johnson put forward an additional idea that may explain the results of the direct-pressure hypothesis—that is, rapid relief of the applied hydrostatic pressure causes a rapid decompression (related to a process called an “ultra-transient microbubble formation”) that affects cell function.
The results of this study will shed light on mechanisms by which elevated intraocular pressure may lead to glaucoma. It is well known that high intraocular pressure can damage the optic nerve in glaucoma, but the precise mechanism by which high pressure leads to the damage is unknown. It presumably involves deformation of the delicate tissues where the optic nerve meets the retina. However, in recent years, an alternate hypothesis has been forwarded that hydrostatic pressure itself can damage ocular tissues, which has led to a variety of studies to assess the effect of pressure on cells and to understand the effects of pressure on cell function.
To date, no studies have been designed to isolate the effects of pressure alone, and none have looked at the effects of rapid depressurization on cells. Drs. Gluckberg and Johnson’s study is designed to control for both the confounding effects of dissolved gas at different pressures and the rate at which pressures are changed. Cell function has been assessed in all of the previous hydrostatic pressure studies after relief of the hydrostatic pressure to which the cells have been exposed.
Drs. Gluckberg and Johnson’s hypothesis is that rapid relief of the applied hydrostatic pressure causes a rapid decompression that affects cell function. If their hypothesis is confirmed, it may help to explain previous experimental results and may lead to further research on the mechanisms by which cells respond to physical stimuli.
About the Researcher
Matthew R. Glucksberg is a Professor of Biomedical Engineering at Northwestern University. His technical expertise is in tissue mechanics, microcirculation, and optical instrumentation. His laboratory has developed image-based instrumentation to measure pressure and flow in the circulation of the eye, instruments to measure the response of pulmonary alveolar epithelial cells to their immediate mechanical environment, and is currently involved in developing minimally invasive optical biosensors for monitoring glucose, lactate, and other measures of metabolic function. He is a co-founder of Northwestern’s Global Healthcare Technologies Program in Cape Town South Africa and co-director of an MS program in Global and Ecological Health.
Dr. Glucksberg is a member of the College of Fellows of the American Institute of Medical and Biological Engineering, a Fellow of the Biomedical Engineering Society, and serves as a founding board member for two non-profit organizations devoted to technology in global health: HealthGreen and the Northwestern Global Health Foundation.
First published on: Monday, July 1, 2013
Last modified on: Thursday, June 27, 2013