Professor of Opthalmology and Vision Science and Pharmacology, Ph.D. University of Arizona, 1996 Biomedical Research Labs B101Dr. Stamer studies the disease of glaucoma, the second leading cause of blindness in the United States, affecting nearly 3 million people. The primary risk factor for developing glaucoma is ocular hypertension (elevated intraocular pressure, IOP). Ocular hypertension is a function of pathology of decreased drainage of aqueous humor from the conventional outflow pathway. Controlling IOP in glaucoma patients, whether or not they have ocular hypertension, is important because results from large clinical trials demonstrate that significant, sustained IOP reduction in people with glaucoma slows or halts vision loss. Therefore, finding new, more effective ways to pharmacologically control IOP is a central goal the Stamer Laboratory.
Using molecular, cellular and organ-based model systems, Dr. Stamer seeks to identify and validate novel drug targets in the human conventional outflow pathway for the treatment of glaucoma.
Z Wan, DF Woodward, C Cornell, H Fliri, J. Martos, S Petit, JW Wang, AB Kharlamb, LAWheeler, ME Garst, K Landsverk, CS Struble, and WD Stamer. Bimatoprost, Prostamide Activity and Conventional Drainage. (2007) Invest. Ophthalmol. Vis. Sci. (in press).
WD Stamer, D Chan, CR Ethier. Targeted Gene Transfer to Schlemm’s Canal by Retroperfusion. (2007) Exp. Eye. Res. 84: 843-849.
D Boassa, WD Stamer and AJ Yool. Ion channel function of Aquaporin-1 natively expressed in choroid plexus. (2006) J. Neuroscience 26: 7811-7819.
SM Conley, BS McKay, AJ Gandolfi, WD Stamer. Alterations in Human Trabecular Meshwork Cell Homeostasis by Selenium. (2006) Exp. Eye Res. 82: 637-647.
KM Hardy, EA Hoffman, BS McKay and P Gonzalez, WD Stamer. Extracellular trafficking of myocilin in human trabecular meshwork cells. (2005) J. Biol. Chem. 280:28917-28926.