Our work in diabetic retinopathy is using high throughput genomic approaches to examine changes in retinal gene expression and epigenetic modifications that are caused by periods of hyperglycemia and are not normalized with restoration of glucose control.
In a second project we are examining deficits in synaptic terminal mitochondrial function as a causative factor in retinal synapse loss with diabetes
Electroretinogram (ERG) scotopic oscillatory potentials (OP) 12-13 weeks post-STZ injection. A) Representative OP traces from non-diabetic (ND – top), diabetic (D – middle), and diabetic with insulin replacement (D+I – bottom) animals showing amplitude ( µV) and time (ms) after dark-adapted light stimulus (-1.4 log(cd s/m2)) at time 0. Numbers (1-4) mark the OPs used for mean and individual implicit time comparison between experimental groups (OP1, OP2, OP3, and OP4). B) Scotopic OP mean implicit time group comparisons for OP1, OP2, OP3, and OP4 between ND (white), D (black), and D+I (gray) animals. * p < 0.05, *** p < 0.001, One-Way ANOVA with Student-Newman-Keuls Method, n=9-11 animals/group. # p < 0.05, Kruskall-Wallis One-Way ANOVA on Ranks with Dunn’s Method, n=9-11 animals/group). From: Functional changes in the neural retina occur in the absence of mitochondrial dysfunction in a rodent model of diabetic retinopathy. Masser DR, Otalora L, Clark NW, Kinter MT, Elliott MH, Freeman WM. J Neurochem. 2017 Dec;143(5):595-608. doi: 10.1111/jnc.14216.