GROWTH MODULATION OF RETINAL MICROVASCULAR CELLS BY EARLY AND ADVANCED GLYCATION PRODUCTS

To investigate the possible implication of non-enzymatic glycosylation in the etiopathogenesis of the diabetic retinopathy, we studied the e ffect of early and advanced glycation products on the growth of retina l microvascular cells. Glucose modified products were obtained by incu bating bovine serum albumin or fetal bovine serum with 0.5 M glucose f or 10 (early glycation products: EG-BSA and EG-FBS, respectively) or 6 0 days (advanced glycation end products: AGE-BSA and AGE-FBS, respecti vely). Cell growth was assessed by cell counting and DNA content deter mination. EG-BSA or AGE-BSA significantly decreased pericyte prolifera tion after 8 days of culture (33 and 13% inhibition, respectively). Co ncerning endothelial cells, EG-BSA reduced proliferation to 40% wherea s AGE-BSA increased it to 156% after 4 days of culture. The glucose-tr eated sera didn't exhibit the same growth effects, neither the EG-FBS nor the AGE-FBS significantly affected endothelial cell proliferation. Only the AGE-FBS showed a significant inhibitory effect on pericyte p roliferation (40% inhibition). We conclude that retinal microvascular cell growth in vitro could be differently modulated by early and advan ced glycation products. The inhibitory effect of AGEs observed on peri cyte growth, suggests that glycoxidation could be implicated in the pe ricyte loss observed in diabetic retinopathy. (C) 1997 Elsevier Scienc e Ireland Ltd.