Haiyan Gong, MD, PhD
PROFESSOR OF OPHTHALMOLOGY AND ANATOMY AND NEUROBIOLOGY
M.D.: Jiangxi Medical College
M.S.: Peking Union Medical College
Ph.D.: Boston University
Postdoctoral Fellowships: West Virginia University & Boston University School of Medicine
Glaucoma is a leading cause of blindness worldwide. A primary risk factor for the development and progression of primary open-angle glaucoma (POAG) is elevated intraocular pressure (IOP), which results from increased resistance to aqueous outflow. However, the cause of this resistance remains unknown. The research in Dr. Gong’s laboratory is to develop new therapeutic strategies to lower IOP in glaucoma, through understanding the mechanisms that regulate aqueous outflow resistance in normal eyes and how this resistance increases in POAG. Dr. Gong’s laboratory has developed a novel fluorophore-guided method of studying the structure and function of the aqueous outflow system. This unique method uses the effective filtration area as a new parameter in examining the structural changes responsible for the reduced outflow in glaucomatous eyes. They are currently using this new method to investigate both the mechanisms of potential new drugs, as well as novel micro-invasive surgical devices in the treatment of glaucoma.
Recently, Dr. Gong’s laboratory is also developing a new approach to investigate how cellular connections of the inner wall endothelial cells of Schlemm’s canal play a role in giant vacuole and pore formation using serial block-face scanning electron microscopy in combination with 3D-reconstruction.
Our current ongoing research projects include:
1. Cellular Physiology of the Aqueous Outflow Pathway
The goals of this project are to determine the factors that regulate the effective filtration area in normal eyes and the changes in these factors responsible for decreased effective filtration area in eyes with ocular hypertension or POAG.
2. The Mechanical Basis of Primary Open Angle Glaucoma
This is a research project in collaboration with Dr. Mark Johnson at Northwestern University. The goal of this project is to determine whether increased stiffness of Schlemm’s canal endothelial cells leads to decreased inner wall porosity and consequently the increased aqueous outflow resistance characteristic of most cases of POAG. Dr. Gong’s laboratory will be involved in morphological studies of this project.
3. Lysosomal Enzymes in Outflow Pathway Physiology and Pathophysiology
This is a research project in collaboration with Dr. Paloma Liton of Duke University. The goals of this project are to demonstrate the existence of a cathepsin B-mediated pericellular and intracellular ECM degradative pathway in trabecular meshwork cells and to investigate the contribution of this degradative pathway on outflow physiology. Dr. Gong’s laboratory will be involved in morphological studies of this project.
4. Effect of Netarsudil on Giant Vacuoles in Schlemm’s canal of perfused Human Eyes
The goal of this research project is to test the hypothesis that one mechanism by which Netarsudil increases trabecular outflow facility is through its effects on increasing the size of giant vacuole along the inner wall of Schlemm’s canal.
5. Effect of AR-12286 on Effective Filtration Area and Morphology of the Trabecular Outflow Pathway
The goal of this research project is to explore the mechanisms of a rho-kinase inhibitor, AR12286 on reduction of IOP in steroid-induced ocular hypertension in mouse eye.