Hui Sun, PhD

Associate Professor, Department of Physiology and Jules Stein Eye Institute, Early Career Scientist, Howard Hughes Medical Institute, David Geffen School of Medicine at UCLA

Research: “Mechanism of tissue inhibitor of metalloproteinase/macular degeneration”

Brief Bio

Dr. Hui Sun is an Associate Professor in the Department of Physiology and at the Jules Stein Eye Institute, David Geffen School of Medicine at UCLA. He is also a member of the Brain Research Institute at UCLA. In 2009, Dr. Sun was selected as one of 50 scientists in the nation to receive the prestigious Early Career Scientist Award from the Howard Hughes Medical Institute.

The E. Matilda Ziegler Foundation provided critical support for Dr. Hui Sun when he started his new lab at David Geffen School of Medicine at UCLA. At that time, one of the main projects of his lab was to build several animal models of age-related macular degeneration (AMD) based on human disease genes associated with early-onset macular degeneration. The human genome project made it possible to perform genome-wide association to identify genes contributing to AMD. These genome-wide studies since 2005 have identified a completely different set of important genes for AMD (e.g., genes involved in innate immunity) and have determined that genes associated with early-onset macular degeneration play minor roles in AMD although their mutations are sufficient to cause macular degeneration in the early-onset forms of the disease. These surprising findings have completely changed the whole field of AMD research.

Dr. Sun’s lab has since contributed to the identification of the functional defect in the human gene most highly associated with AMD (complement factor H, CFH). His lab found that the AMD-associated polymorphism in CFH has almost completely abolished its binding to its receptor on Streptococcus pyogenes, a major human pathogen that historically caused significant mortality in human populations. This is one of the rare examples of a dramatic phenotype for a very common human polymorphism. This finding has implications in the evolutionary driving forces to preserve this polymorphism (and its linked SNPs) in human populations. His lab is continuing to determine the functional consequences of human polymorphisms associated with AMD. Only when the functional consequence is known, can the detailed molecular pathway be revealed.