Jerry G. Webb
Jerry Webb, Ph.D.
1972 Ph.D., University of Utah
Cellular Mechanisms in the Regulation of Intraocular Pressure
Elevated intraocular pressure is a major risk factor in glaucoma, the most common cause of irreversible blindness worldwide. The Webb laboratory is interested in endogenous mechanisms that contribute to the physiological regulation of intraocular pressure, and in defining factors that contribute to the pathophysiological pressure rise in glaucomatous individuals. Studies are focused on actions of the kallikrein/kinin system that we have found to increase outflow of aqueous humor within the anterior chamber of the eye. We have also observed that bradykinin synergistically enhances PGE2 signaling in trabecular meshwork cells, an interaction that may contribute significantly to the regulation of outflow resistance.
The objectives of current studies are to determine the mechanism of kinin/PGE2 signal interactions in trabecular meshwork cells, and the contribution of these interactions to the regulation of aqueous outflow. Emphasis is on the importance of effector isoforms as focal points of signal integration. Experiments are performed with isolated perfused bovine and human anterior segments and with cultured cell models from bovine and human eyes using biochemical and molecular probes.
1. Webb, J.G., et al., Bradykinin activation of extracellular signal-regulated kinases in human trabecular meshwork cells, Experimental Eye Research (2011), doi:10.1016/j.exer.2011.03.009
2. Webb J.G., Yang X. and Crosson C.E. Expression of the Kallikrein/Kinin System in Human Anterior Segment. Exp Eye Res. 89:126-132, 2009.
3. Webb J.G., Husain S., Yates P.W. and Crosson C.E. Kinin Modulation of Conventional Outflow Facility in the Bovine Eye. J. Ocular Pharmacol Therap. 22:310-316, 2006.
4. Webb J.G., Shearer T.W., Yates P.W., Mukhin Y.V. and Crosson C.E. Bradykinin Enhancement of PGE2 Signalling in Bovine Trabecular Meshwork Cells. Exp Eye Res. 76(3):283-9, 2003.