The precise pathogenic mechanisms that lead to retinal ganglion cell (RGC) death in glaucoma is unknown. Despite the vulnerability of RGCs in glaucoma, glial cells located in the optic nerve head, or retina, survive glaucomatous stress. Dr. Tezel has hypothesized that this different susceptibility to damage is due to differential activity of signaling cascades in these cell types. To determine the validity of this hypothesis, he is conducting in vitro cell culture experiments with each cell type separately and in co-culture to examine the signaling cascades in response to elevated hydrostatic pressure. He will also determine the activation of specific kinases in an in vivo rat model of high-pressure glaucoma, and in human donor eyes affected by glaucoma. It is hoped that the information gained from these studies will help describe the mechanisms determining the fate of cells in response to glaucoma, and may provide targets for possible new drugs to treat the condition.
First published on: June 10, 2008
Last modified on: June 11, 2008