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Growth modulation of retinal microvascular cells by early and advanced glycation products
D Ruggiero-Lopez1, N Rellier, M Lecomte
1Diabetic Microangiopathy Unit, LIPHA-INSERM U352, INSA-Lyon, France.ruggiero@insa.insa-lyon.fr
Abstract:
To investigate the possible implication of non-enzymatic glycosylation in the etiopathogenesis of the diabetic retinopathy, we studied the effect of early and advanced glycation products on the growth of retinal microvascular cells. Glucose modified products were obtained by incubating bovine serum albumin or fetal bovine serum with 0.5 M glucose for 10 (early glycation products: EG-BSA and EG-FBS, respectively) or 60 days (advanced glycation end products: AGE-BSA and AGE-FBS, respectively). Cell growth was assessed by cell counting and DNA content determination. EG-BSA or AGE-BSA significantly decreased pericyte proliferation after 8 days of culture (33 and 13% inhibition, respectively). Concerning endothelial cells, EG-BSA reduced proliferation to 40% whereas AGE-BSA increased it to 156% after 4 days of culture. The glucose-treated 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 proliferation (40% inhibition). We conclude that retinal microvascular cell growth in vitro could be differently modulated by early and advanced glycation products. The inhibitory effect of AGEs observed on pericyte growth, suggests that glycoxidation could be implicated in the pericyte loss observed in diabetic retinopathy.
Insights
Non-enzymatic glycosylation impacts diabetic retinopathy. Early and advanced glycation products differentially affect retinal microvascular cell growth, with advanced glycation end products inhibiting pericyte proliferation, suggesting a role in diabetic retinopathy pathogenesis.
Area of Science:
- Ophthalmology
- Endocrinology
- Cell Biology
Background:
- Diabetic retinopathy is a leading cause of vision loss.
- Non-enzymatic glycosylation is implicated in diabetic complications.
- The specific effects of glycation products on retinal microvasculature require further investigation.
Purpose of the Study:
- To investigate the role of early and advanced glycation products (EGPs and AGEs) in diabetic retinopathy pathogenesis.
- To determine the effects of EGPs and AGEs on retinal microvascular cell growth in vitro.
Main Methods:
- Bovine serum albumin (BSA) and fetal bovine serum (FBS) were incubated with glucose to create EGPs and AGEs.
- Retinal microvascular endothelial cells and pericytes were cultured with these glycation products.
- Cell proliferation was assessed using cell counting and DNA content determination.
Main Results:
- EG-BSA and AGE-BSA significantly inhibited pericyte proliferation.
- EG-BSA reduced endothelial cell proliferation, while AGE-BSA increased it.
- Glucose-treated sera showed varied effects; AGE-FBS significantly inhibited pericyte proliferation.
Conclusions:
- Early and advanced glycation products differentially modulate retinal microvascular cell growth in vitro.
- The inhibitory effect of AGEs on pericyte growth suggests a potential role in the pericyte loss seen in diabetic retinopathy.
- Glycoxidation may be a key factor in the development of diabetic retinopathy.