Please join Sayon Roy, PhD, Boston University, for a presentation entitled “Breakdown of Vascular Homeostasis in Diabetic Retinopathy.” The lecture will take place on April 4, 2017 as part of the Research Lecture Series. All are welcome to attend. One hour of Mass CE will be awarded.
Please join us for a wine and cheese reception in Conference Room 1 following the lecture.
Abstract: Global increase in the diabetic population forecasts a significant rise in the number of individuals with diabetes-related retinal diseases. This combined with a dramatic rise in the aging population could impact the overall incidence and prevalence of diabetic retinopathy. An overwhelming cause of vision loss in diabetic individuals is the breakdown of retinal vascular homeostasis, contributing to excess permeability and the development of macular edema, a prominent clinical manifestation of diabetic retinopathy. Despite the use of laser photocoagulation, and available therapeutics, majority of the patients do not fully recover functional vision. Research into areas involving cell-cell communication and blood retinal barrier characteristics has uncovered a significant underlying factor that contributes to both these functional changes. Our studies indicate that abnormal thickening of the vascular basement membrane (BM) can contribute to excess vascular permeability, breakdown in cell-cell communication, and retinal vascular cell loss. The latter has also been observed in aging. It has long been established that vascular BM thickening is a characteristic hallmark of diabetic microangiopathy, however, it is unclear how vascular BM thickening promotes the characteristic lesions seen in diabetic retinopathy, and whether aging affects retinal vascular lesions characteristic of diabetic retinopathy. Recent studies have begun to shed light on this subject suggesting vascular BM thickening as a key player that not only compromises the BRB characteristics but also affects vascular homeostasis and promotes cell loss associated with the development and progression of diabetic retinopathy. Importantly, our research has identified several BM genes, fibronectin, collagen IV, and laminin that are abnormally expressed under hyperglycemic condition and contribute to abnormal cell-cell communication and retinal vascular leakage. Furthermore, retinal vascular changes that develop during aging appear to resemble lesions characteristic of diabetic retinopathy. A strategy for decreasing retinal vascular BM thickening and understanding how this could prevent vascular complications and contribute to the maintenance of vascular homeostasis in the diabetic retina will be the focus of the presentation.