Immune cells play important roles in retinal vascular development/remodeling/repair and degeneration. Immune dysregulation during these processes in the eye leads to diseases such as retinopathy of prematurity and age-related macular degeneration. Our research interests focus on the roles of immune-vascular interaction and neuroinflammation in the development of vascular eye disorders and retinal degeneration using genetically modified mouse models and disease models, and developing effective ways to treat or prevent vision loss.
Current research projects in our lab include:
The mechanisms of immune-vascular crosstalk in controlling retinal angiogenesis.
We aim to investigate the molecular mechanisms of master immune regulator, SOCS3 in immune cells in modulating inflammatory signals to control immune-vascular crosstalk in retinopathy, and target this novel factor to design new therapeutic approaches for treating vascular eye diseases including retinopathy of prematurity and age-related macular degeneration.
Photoreceptors determination of retinal blood vessel growth in retinopathy through neuroinflammation.
Our recent work leads to the important finding that neuroinflammatory signals in normally avascular photoreceptor layer modulated by transcription factor c-Fos can regulate retinal neovascularization. Our lab focuses on the roles of c-Fos pathway as a major signaling pathway that used by stressed photoreceptors to convey a need for blood vessels and as a potential upstream target to control the development of retinal angiogenesis through neuroinflammation.
- Microglia and immune regulation in photoreceptor development and degeneration.
Center for Life Sciences Building, Room 18045
300 Longwood Ave.
Boston, MA 02115