Glaucoma is the leading cause of irreversible blindness worldwide and is characterized by a specific pattern of retinal ganglion cell (RGC) loss; however, pathogenic mechanisms of this disease are not fully understood. At present, the sole modifiable risk factor for glaucomatous RGC loss is intraocular pressure (IOP), and current therapeutic strategies aim to lower IOP. Our research focuses on understanding why RGCs are susceptible to IOP in glaucoma, and how we can prevent vision loss independent of IOP.

Investigating glial and neuronal mechanosensation in glaucoma

Studies have shown that the site of RGC injury in glaucoma occurs at the optic nerve head (ONH). The ONH contains an extracellular matrix (ECM) network, astrocytes, and microglia that all work to support RGC axons as they exit the eye. We use various bioreactors to apply biomechanical forces to these components of the ONH to learn how they sense these forces. By focusing on mechanosensitive channels (which include Transient Receptor Protein; TRP channels and Piezo channels), we are working to prevent ONH damage even when IOP is elevated.

Engineering a 3-dimensional hydrogel platform to study the optic nerve head

We need to better understand how cells of the optic nerve head interact to get at how these cells are dysfunctional in glaucoma. There is increasing evidence to support that astrocytes and microglia respond to biomechanical strains by altering their signaling profile. We use primary glial cells from mice and incorporate them into our hydrogel system. We then test how they respond to various glaucomatous stressors. Cells within our hydrogel matrix behave more closely to in vivo than on 2D culture, making this an ideal tool to study cellular behavior in glaucoma.

Education & Fellowships

Fellowship: Duke Eye Center, 2018, Glaucoma
Residency: Cleveland Clinic Cole Eye Institute, 2017, Ophthalmology
Internship: Augusta University, 2014, Medicine
MD: Augusta University, 2013
PhD: Augusta University, 2013, Cellular Biology