Boston University School of Medicine
Title: Role of intercellular communication in diabetic retinopathy
Sayon Roy received his PhD from Boston University and completed his postdoctoral training at Harvard Medical School, Harvard University. Dr. Roy is currently a professor of Medicine, Section of Diabetes, Endocrinology and Nutrition, and a professor of Ophthalmology at Boston University School of Medicine. Recognized as an expert in retinal vascular biology, Dr. Roy’s seminal work led to the identificationof several genes in the retina that are abnormally expressed in diabetic retinopathy. His pioneering work resulted in the development of novel gene modulatory techniques in retinal vascular cells using antisense oligonucleotides via intravitreal injection. Dr. Roy has received numerous awards including the American Diabetes Association Research Award for the commitment and dedication towards the fight against diabetes, the 2006 Mentor of the Year Award from Boston University, and the 2008 Innovative Award from the Juvenile Diabetes Research Foundation. Research in Dr. Roy’s laboratory has been funded by several organizations including the National Eye Institute, NIH, National Medical Technology Testbed,American Diabetes Association, Juvenile Diabetes Research Foundation International, Fight for Sight, Research to Prevent Blindness, and the Lions Organization. Dr. Roy has been a chartered member of the NEI Study Section of the National Institutes of Health.
Breakdown of the blood-retinal barrier (BRB) is a prominent pathophysiological event in diabetic retinopathy diabetic retinopathy. Studies have linked this cellular event to be regulated, at least in part, by reduced expression of tight junction proteins. Recent studies suggest that connexin 43 (Cx43), a gap junction protein, is required to maintain endothelial barrier function. However,its role in retinal vascular leakage is currently unknown. In this presentation, the importance of cell-to-cell communication in diabetic retinopathy will be discussed. In particular, the effects of high glucose and diabetes on Cx43 expression, and how breakdown in cell-cell communication in diabetes promotes retinal vascular abnormalities in diabetic retinopathy will be presented. Additionally the relationship between gap junctions and tight junctions in the context of vascular permeability in diabetic retinopathy will be highlighted. Overall, our findings indicate that hyperglycemia-induced Cx43 downregulation compromises retinal vascular homeostasis, compromises BRB, and promotes vascular lesions.