Page 48 - AWSAR 2.0

24 || AWSAR Awarded Popular Science Stories - 2019
indeed neurons. Next, we established a model of hyperglycemia (high glucose) by culturing retinal cells in high (25 mmol/L glucose equivalent to blood sugar levels of 450 mg/dL) or normal concentration of glucose (5 mmol/L glucose, equivalent to normal fasting blood sugar levels of 90 mg/dL).
Using our model of hyperglycemia, we then studied the effect of high glucose levels on CAMs present on the surface of retinal neurons. We also examined the effect of high glucose levels on the length of processes (neurites) extending from the cell bodies of the neurons. Our experiments demonstrated that high glucose levels resulted in a substantial increase in neurite length in cultured retinal neurons. Excess glucose in the nutrient medium also leads to a significant decrease in the levels of neuronal CAMs such as Caspr, contactin, and prion proteins. Hyperglycemia
was also found to alter the level of a glucose homeostasis-sensitive transcription factor calledC/EBPα,whichmightregulatethegene expression of CAMs in the neuronal nucleus. Further detailed experiments will be performed to confirm these findings.
In conclusion, we have described a unique model of hyperglycemia in higher mammals using adult goat retinal culture. This approach can be used to perform additional systematic studies on neurons and explore the effects of high glucose levels on signaling pathways involved in neurite extension. Our studies using this model may, thus, facilitate the identification of fundamental mechanisms underlying neurodegenerative diseases such as DR in higher mammals, which cannot be revealed through studies in rodent-derived cells.