Abstract
Purpose :
Diabetic retinopathy is one of the three major complications of diabetes together with diabetic neuropathy and nephropathy, and it is an important disease as a cause of blindness. Diabetes-induced retinal dysfunction can be detected by electroretinogram (ERG). It is known that oscillatory potential (OP), which is thought to be derived from amacrine cells detected by ERG, attenuates early in diabetes. On the other hand, there are reports suggesting that attenuation of OPs in diabetic retinopathy is related to reduced neuroprotective factors. Therefore, we focused on the expression of brain-derived neurotrophic factor (BDNF), one of the neuroprotective factors, in the retina, and examined its role in diabetic retinopathy and the possibility of further treatment. We also examined whether eicosapentaenoic acid (EPA) and its metabolite elevate BDNF expression in the diabetic retinopathy.
Methods :
We examined the cell viability of MIO-M1 cells (Müller cell origin) cultured in high glucose medium and PC12D cells (retina neuronal cells) by WST-1 assay and BDNF expression of MIO-M1 cells by RT-PCR. Thereafter, BDNF was administered to PC12D cultured in high glucose medium and WST-1 was performed. Furthermore, the expression of BDNF was again evaluated after resolvin E1 (RvE1), one of the metabolites of EPA, was administered to MIO-M1 cells under high glucose condition.
Results :
Under high glucose condition, cell viability was decreased in both MIO-M1, and BDNF expression of MIO-M1 cells was decreased. On the other hand, administration of BDNF increased cell viability of PC12D cells. In addition, when the RvE1 was administered to MIO-M1 cells under high glucose condition, the expression of BDNF was significantly improved.
Conclusions :
These in vitro experiments suggested that retinal dysfunction observed in diabetic retinopathy is related with the BDNF reduction in Müller cells.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.