OUR RESEARCH
The central goal of our lab is to prevent blinding eye disease. Our research is focused on promoting regenerative healing in the eye after wounding and treating glaucoma by targeting the cellular dysfunction that promotes disease progression. We are interested in the involvement of aberrant protein aggregation and ubiquitin-mediated pathways in these pathologies.
Regenerative Healing in the Eye
We have elucidated novel intracellular ubiquitin-mediated degradation pathways that control cell-surface integrin expression and subsequent fibrotic growth factor (TGFb) signaling and scarring in the eye. We are using the cornea as a model system because corneal transparency is critical for clear, unobstructed vision, making it an important tissue in which to study scarring. The cornea refracts light as it enters the eye so that a properly focused image reaches the retina. When a cornea is wounded by surgery or injury, the wound may heal in a regenerative process (no scarring) or may enter a progressive loop of fibrosis (scarring). Our goal is to understand the mechanisms that promote regenerative wound healing and to apply these findings not only to the cornea, but to other models of fibrotic disease.
Autophagic Dysfunction in Exfoliation Glaucoma
Our work on Exfoliation glaucoma (XFG) also has broad consequences for the prevention of blindness. In XFG, the leading identifiable cause of glaucoma, the eye accumulates protein aggregates that block the exit of fluid from the eye. This project interrogates the basic mechanisms leading to protein aggregate formation and expulsion from cells, including protein folding mechanisms, mitochondrial health, microtubule dynamics, and autophagic pathways. The primary cells in combination with a new XFG mouse model are being utilized to understand the mechanistic underpinnings of the disease and to test novel therapies that may interrupt and reverse XFG disease processes.
