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Cristian Mercado, Andrew T C Tsin; Effect of glucose on cultured mouse cone photoreceptor cell viability and VEGF secretion. Invest. Ophthalmol. Vis. Sci. 2018;59(9):5353. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Some degree of photoreceptor degeneration may occur in early stages of diabetes and prior to the onset of diabetic retinopathy (DR). Such event may contribute to the development of DR. The aim of this study is to investigate the effect of distinct glucose concentrations over the mouse cone photoreceptor 661W cell viability and vascular endothelial growth factor (VEGF) secretion.
Photoreceptor cells were seeded at 20,000 per well in a 24 wells plate. Cells were cultured with glucose concentrations of 0 mM (hypoglycemic), 5 mM (euglycemic), 18.5 mM, and 30 mM (hyperglycemic) for 24 hours. Cell viability was determined by trypan blue dye exclusion method and VEGF levels in culture media were measured by ELISA.
High glucose concentrations (30 mM) decreased the number of viable cells by 11% compared to the physiological control (5 mM; X=11,250; N=3) after 24 hours of treatment. In comparison, cell viability increased by 50% in 18 mM glucose and decreased by 74% in the absence of glucose (0 mM). In contrast, VEGF levels in conditioned media increased with glucose concentration (8, 16 and 28 pg/ml VEGF in 0, 5.5 and 18.5 mM glucose respectively) but decreased to 16 pg/ml at 18.5 mM glucose. However, VEGF levels per viable cell showed an inverse relationship with 0mM glucose at the highest ratio of 2.7 pg VEGF/1000 cells.
Our results are consistent with previous reports that glucose affects cell viability and VEGF secretion of multiple ocular cells. Our data highlights the role of extracelluar glucose levels in angiogenesis and the development of DR. These results reveal for the first time a possible involvement of cone photoreceptor cells on the development of DR.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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