Conclusions
Elevated glucose decreased HRP viability and modulated changes in TGFbeta2 and VEGF release. This suggests a novel mechanism for HRP dropout in diabetic retinopathy.
Methods
Human retinal pericytes (HRP) were cultured in 5 mM (physiologic) or high (18 mM) glucose with or without added TGFbeta2. Viable cells were counted; TGFbeta2 and VEGF in the conditioned media (CM) were measured by ELISA.
Purpose
Determine the effects of glucose and exogenous TGFbeta2 on viability and VEGF release by human retinal pericytes (HRP).
Results
High glucose significantly reduced viable cell number and increased the levels of TGFbeta2 and VEGF. TGFbeta2 caused a significant dose-dependent effect on viable cell number and on the level of VEGF secreted into the CM by HRP in physiologic glucose, decreasing viable cell number, and increasing VEGF release per 1000 cells at a low concentration (0.1 ng/ml) and increasing viable cell number and decreasing VEGF release per 1000 cells at higher concentrations (1.0 and 10 ng/ml). TGFbeta2 affected neither parameter in high glucose. Conclusions: Elevated glucose decreased HRP viability and modulated changes in TGFbeta2 and VEGF release. This suggests a novel mechanism for HRP dropout in diabetic retinopathy.