Sayon Roy received his Ph.D. from Boston University and completed his postdoctoral training at Schepens Eye Research Institute, 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 has identifi ed several genes in the retina that are abnormally expressed in diabetic retinopathy. His pioneering work has led to 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 fi ght 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 currently serves as a chartered member of the NEI Study Section of the National Institutes of Health.


Diabetic retinopathy is the leading cause of blindness in the working age population for which unfortunately there is no preventative therapy. Chronic hyperglycemia is a major inducer of diabetic retinopathy in both type 1 and type 2 diabetes. Ultrastructural and cellular changes in the retinal vessels are closely associated with the development of diabetic retinopathy. The thickening of the basement membrane (BM) in the small blood vessels of the diabetic retina is a prominent and characteristic ultrastructural change that affects cellular function during the pathogenesis of diabetic retinopathy. Several years of research has established hyperglycemia, the most prevalent characteristic of diabetes, as a primary causal factor mediating this alteration. Studies have established the negative impact of hyperglycemia on the pathogenesis of diabetic retinopathy; however, the specific cellular mechanisms that lead to the dysfunction of small vessels in diabetes are unclear. In particular, it is unknown how vascular BM thickening promotes serious structural and functional abnormalities in the diabetic retina. While the association between BM thickening and the development and progression of diabetic retinopathy has been observed long ago, only recently new evidences have come to light that indicate vascular BM thickening plays a causal role in the pathogenesis of diabetic retinopathy. Our research has identified several BM genes, fibronectin, collagen IV, laminin, and cellular events involving connexin-43 gap junction intercellular communication that are significant players in mediating hyperglycemia-driven vascular lesions. Additionally cell-cell communication is notably altered in diabetic retinopathy. These novel changes play a significant role in promoting characteristic vascular lesions during the pathogenesis and progression of diabetic retinopathy.

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