Directional Exosome Proteomes Reflect Polarity-Specific Functions in Retinal Pigmented Epithelium Monolayers.

My research focuses on applying mass spectrometry based proteomics to study proteins in eye tissues, cells and sub-cellular compartments to understand mechanisms of vision. An important aspect of my research is to identify proteins in different compartments of retinal photoreceptor cells, their amount and modification status at different cell states defined by the light conditions, genotype, disease etc. This information can be valuable in understanding molecular mechanisms of vision and biology of the photoreceptor cell. Another important aspect of my research is to assist basic scientist and clinicians in our department in their proteomic needs which include identification of proteins and other biomolecules in a given biological sample, detection of protein post-translational modifications and sequence variations, elucidation of protein-protein interactions and also characterization of changes in the protein concentration and composition in a biological sample at different conditions.

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 the regulated movement of aqueous humor into and out of the eye.  Elevated IOP in glaucoma is a result of disease in the primary efflux route, the conventional outflow pathway, affecting proper homeostatic control of aqueous humor drainage.

Lowering 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 first-line 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 medically control IOP by targeting the conventional pathway is a central goal the Stamer Laboratory.

Using molecular, cellular, organ and mouse model systems, my laboratory seeks to identify and validate novel drug targets in the human conventional outflow pathway to facilitate the development of the next generation of treatments for ocular hypertension and glaucoma.

Dr. Bowes Rickman is a highly accomplished translational scientist whose research efforts over two decades have been focused on the molecular/cell biology and pathobiology of age-related macular degeneration (AMD). In an effort to better understand the pathophysiology of AMD, she has created a number of murine models that recapitulate many aspects of human AMD and point the way toward eventual treatments for AMD. Among many cited seminal contributions is her discovery of a connection between complement and lipoprotein metabolism and AMD and the development of a murine model that closely mirrors findings in humans. Using these models, Dr. Bowes Rickman has dissected disease mechanisms that contribute to AMD risk, and tested multiple novel therapeutic targets for its treatment.