William D Stamer
Joseph A.C. Wadsworth Professor of Ophthalmology
Appointments and Affiliations
- Joseph A.C. Wadsworth Professor of Ophthalmology
- Professor of Ophthalmology
- Office Location: 2608 Erwin Rd, Box 148-145, Durham, NC 27705
- Office Phone: (919) 684-3745
- Email Address: email@example.com
- University of Arizona College of Medicine, 2011
- University of Arizona College of Medicine, 2006
- University of Arizona College of Medicine, 2003
- Duke University School of Medicine, 1998
- University of Arizona College of Medicine, 1997
- University of Arizona College of Medicine, 1996
- Ph.D. University of Arizona, 1996
- B.S. University of Arizona, 1990
Research InterestsThe Mechanobiology of Ocular Hypertension in Glaucoma: My laboratory studies the disease of glaucoma, the second leading cause of blindness in the United States, affecting nearly 3 million people (70 million Worldwide). The primary risk factor for developing glaucoma is ocular hypertension (high intraocular pressure, IOP). IOP is a function of aqueous humor moving into and out of the eye. Elevated IOP in glaucoma is a result of disease in the primary efflux route, the "pressure-sensitive" conventional outflow pathway. Controlling IOP in glaucoma patients, whether or not they have ocular hypertension, is important because large clinical trials involving tens of thousands of patients repeatedly demonstrate that significant, sustained IOP reduction slows or halts vision loss. Unfortunately, current daily medical treatments do not target the diseased conventional pathway and do not lower IOP sufficiently in most people with glaucoma. Therefore, finding new, more effective ways to control IOP by targeting the conventional pathway is a central goal the Stamer Laboratory. Using molecular, cellular, organ and living model systems, my laboratory seeks to better understand the mechanobiology of conventional outflow with the ultimate goal to identify and validate targets in the conventional outflow pathway such that novel treatments for ocular hypertension and glaucoma can be developed. We study the dynamic mechanical behavior of the conventional outflow cells and tissues using a variety of approaches including optical coherence tomography, atomic force microscopy, cellular dielectic spectroscopy, ocular perfusions, mechanical stretch and contractility assays.
- Elliott, MH; Ashpole, NE; Gu, X; Herrnberger, L; McClellan, ME; Griffith, GL; Reagan, AM; Boyce, TM; Tanito, M; Tamm, ER; Stamer, WD, Caveolin-1 modulates intraocular pressure: implications for caveolae mechanoprotection in glaucoma, Scientific Reports, vol 6 (2016), pp. 37127-37127 [10.1038/srep37127] [abs].
- Ren, R; Li, G; Le, TD; Kopczynski, C; Stamer, WD; Gong, H, Outflow facility in human eyes through multiple mechanisms, Investigative Ophthalmology and Visual Science, vol 57 no. 14 (2016), pp. 6197-6209 [10.1167/iovs.16-20189] [abs].
- Dismuke, WM; Klingeborn, M; Stamer, WD, Mechanism of Fibronectin Binding to Human Trabecular Meshwork Exosomes and Its Modulation by Dexamethasone, PloS one, vol 11 no. 10 (2016), pp. e0165326-e0165326 [10.1371/journal.pone.0165326] [abs].
- Paula, JS; O'Brien, C; Stamer, WD, Life under pressure: The role of ocular cribriform cells in preventing glaucoma, Experimental Eye Research, vol 151 (2016), pp. 150-159 [10.1016/j.exer.2016.08.014] [abs].
- Dismuke, WM; Overby, DR; Civan, MM; Stamer, WD, The Value of Mouse Models for Glaucoma Drug Discovery, Journal of Ocular Pharmacology and Therapeutics, vol 32 no. 8 (2016), pp. 486-487 [10.1089/jop.2016.29010.mjc] [abs].