Epigenetic Prevention of AMD Progression by Vitamin C
Currently, the first-line treatment for wet AMD is to block the function of vascular endothelial growth factor (VEGF), a major factor promoting the growth of new blood vessels in the eye. Besides the high costs, these treatments are injected into the eyeball using syringes, which is complicated and can be dangerous. Based on a novel finding from our lab, that ascorbate (vitamin C) plays a role in regulating the function of the genome, this research aims to use vitamin C to inhibit the production of VEGF in the eye, thus blocking its function. Successful completion of this research will help develop an ascorbate treatment to delay and/or prevent disease progression that is inexpensive and readily available for AMD patients.
This research aims to develop a prevention of AMD by vitamin C (ascorbate), which may inhibit intraocular VEGF signaling. We will first examine the effect of ascorbate on VEGF expression in human retinal pigmented epithelium (RPE) cells. The mechanism by which ascorbate inhibits VEGF will be examined by high-throughput sequencing technology. After that, ascorbate will be tested in modeled mice to see if VEGF overexpression and choroidal neovascularization can be prevented by the treatment. Currently, the first-line treatment for wet AMD is to block the function of VEGF, a major factor promoting the growth of new blood vessels in the eye. These treatments are costly and complicated to perform, requiring injections into the eyeball. Furthermore, anti-VEGF therapies only temporarily block the action of VEGF, but have no effect on the continued production of VEGF within the eye. Based on a novel finding from our lab, of ascorbate’s ability to regulate the function of the genome, this research aims to use vitamin C to inhibit the production of VEGF in the eye, thus blocking its function. Successful completion of this project will help to develop an ascorbate treatment to delay and/or prevent AMD progression that is inexpensive and readily available for AMD patients
About the Researcher
After earning my PhD in physiology at the Fourth Military Medical University in China, I started my postdoctoral training at Duke University, first working on G protein–coupled receptor (GPCR) signaling and then Parkinson’s disease. Since 2007, my independent research has been focused on the functional genomics of age-related macular degeneration (AMD), especially the function of the chromosome 10q26 locus in AMD development. I was fortunate enough to be funded by the BrightFocus Foundation to carry out research on a detailed examination of the ARMS2 gene (the gene that codes for age-related maculopathy susceptibility protein 2, which is thought to play a role in AMD). Currently, my research focuses on the epigenetic regulation of vitamin C in different diseases, including AMD.
As a trained bench scientist, I always feel most relaxed and excited to conduct the so-called “wet lab” experiments that involve looking at cells and tissues under a microscope. Alas, now I spend most of my time staring at a computer monitor in a small office. Like other principal investigators, my job is confined to writing either grant proposals or manuscripts. I love writing, but I don’t like to stare at a monitor all day long because my right eye is starting to fail me. If you’re not careful or protective, your eyes may fail you too. Every day while riding the metro, I see the people around me all glued to their flashy phones and bright-screened devices. I can’t tell people to stop using these fancy technologies, but perhaps I can help develop a way to delay or even prevent the onset of AMD, one of most common diseases of vision loss. With the support of the BrightFocus, I am dedicated to test whether vitamin C can be such a prevention.
First published on: August 15, 2017
Last modified on: June 30, 2020