The Department of Ophthalmology’s research mission is strengthened by the addition of several new faculty members
- Christine N. Kay, MD. was appointed as Assistant Professor of Ophthalmology in the Fall of 2011. She graduated magna cum laude with a B.A. in Neurobiology from Harvard University in 2001, and then completed her medical degree at the University of Florida College of Medicine in 2005. After completing a transitional internship at the Roanoke Carilion Memorial Hospital, she completed her Ophthalmology residency training at the University of South Florida, and a vitreoretinal fellowship at the University of Iowa. Dr. Kay is board certified by the American Board of Ophthalmology and is a member of the American Academy of Ophthalmology and the American Society of Retinal Specialists. Dr. Kay evaluates and treats multiple retinal problems including diabetic eye disease, retinal vascular occlusions, macular edema, uveitis, macular degeneration, epiretinal membranes and macular holes, retinal tears and detachments, and has a particular interest in inherited retinal disease and electrophysiology. She is the director of the electrophysiology service and director of the vitreoretinal fellowship. Her particular research focus is in gene therapy delivery for inherited retinal disease. She has a career development award from the Foundation Fighting Blindness for research on genetic therapy for Achromatopsia, a disease affecting color vision and central vision.
- Qiuhong Li, Ph,D. was appointed as Associate Professor in the Fall of 2011. Her research interest surrounds diabetic retinopathy, the leading cause of severe vision loss in people under age of sixty. Dr. Li’s research goal is to understand the pathogenesis of diabetic retinopathy and to develop more effective therapies for treatment of this condition, with a particular focus on the targeting ocular renin angiotensin system. The renin angiotensin system, as a fundamental regulator of cardiovascular homeostasis and a key contributor in cardiovascular diseases, is also produced locally in the eye. Funded by American Diabetes Association, American Heart Association and NIH, her research projects include (1) investigating the role and mechanisms of ocular renin angiotensin system in development and progression of diabetic retinopathy; (2) the protective role and mechanisms of recently established new axis of the renin angiotensin system: ACE2/Ang 1-7/Mas in diabetic retinopathy, using both gene-based and pharmacological approaches in animal models as well as in vitro studies.
- John Ash, Ph.D. was appointed as Associate Professor in the Fall of 2011. Dr. Ash’s research is focused on both understanding the cause of blindness due to retinal degeneration and developing therapies to prevent loss of sight. His research is relevant to inherited retinal degenerations such as retinitis pigmentosa, cone-rod dystrophies, LCA, or age related macular degeneration. His most recent studies have shown the important contribution of endogenously expressed cytokines such as leukemia inhibitory factor (LIF). His work has shown that these cytokines are expressed under conditions of stress, and that the increased LIF is important to prevent or delay photoreceptor or RPE cell death under chronic stress conditions, including inherited mutations known to cause blindness. By using mouse genetic engineering, his lab has demonstrated that loss of the LIF receptor, gp130 or it’s signaling intermediate STAT3, results in accelerated retinal degeneration. The results from this work have broad implications in the understanding of human inherited retinal degeneration. In humans, disease-causing genes are present before birth; however patients inheriting those mutations that cause retinitis pigmentosa or age related macular degeneration typically do not develop disease for 40 to 80 years. Dr. Ash’s work suggests that LIF and its receptor gp130 keep cells alive and functioning, and serve to delay the onset and progression of disease. Variation in efficiency of this internally protective activity could also be a partial explanation of why family members who inherit the same mutation can have a wide range in the age of onset and severity of disease. This work has led to the identification of drug targets to promote cell survival, and has led to the development of several gene therapy approaches to specifically enhance the survival of photoreceptors and RPE which are now being tested in models of disease.
- Shannon E. Boye, Ph.D. was appointed as Assistant Professor in the Fall of 2012. Her expertise lies in the use of viral vectors to treat inherited retinal disease. Her appointment both strengthens the foothold and supports the University of Florida’s continued presence in this exciting area of research. Dr. Boye’s lab currently focuses heavily on three areas of research. (1) Develop a treatment for GUCY2D Leber congenital amaurosis (LCA1). The lab has already demonstrated the ability to restore retinal function and visually-guided behavior and preserve retinal structure in several animal models of this devastating early-onset retinal dystrophy. Dr. Boye is now moving beyond this proof-of-concept work and is developing a clinical-grade AAV vector with which to perform safety studies. Dr. Boye and her collaborators are hopeful that this treatment will be applied to patients within a couple of years. (2) Optimize AAV vectors to target genes to photoreceptors following intravitreal injection. Because most retinal degenerations are caused by mutations in photoreceptor-specific, rather than RPE-specific, genes, there is a great need to develop photoreceptor-targeted gene therapies. Of equal importance is the need to develop an injection procedure which is less invasive than the state of the art (subretinal injection), particularly when an underlying genetic defect leads to a degenerative process and a fragile retina prone to further damage upon surgically induced retinal detachment. Using both rational mutagenesis and directed evolution techniques, the Boye lab seeks to develop AAV vectors that possess an ehanced ability to transduce photoreceptor cells, notably foveal cones, following intravitreal delivery. (3) Expand AAV vector technology. The Boye lab is actively developing novel dual AAV vector platforms which are capable of delivering large transgenes. Once thought to be a limiting factor for AAV gene delivery, this technology will allow for the treatment of many diseases associated with mutations in large genes (>~5kb). Specific emphasis is placed on myosinVIIa Usher syndrome (USH1b) and congenital stationary night blindness.