Neurodegeneration: An early event of diabetic retinopathy

Figure 1 Comparison of the two key elements of neurodegeneration (glial activation and apoptosis) between a representative case of diabetic patient without DR and a non-diabetic subject. As can be seen, neurodegeneration is higher in the retina from the diabetic donor. A: Glial activation in the human retina. Glial fibrillar acidic protein (GFAP) immunofluorescence (green) from a non-diabetic donor (left panel) and a diabetic donor (right panel); B: Apoptosis in the human retina. Upper panel: Non-diabetic donor (B1: Propidium iodide, B2: TUNEL immunofluorescence). Low panel: Diabetic donor (B3: Propidium iodide, B4: TUNEL immunofluorescence). RPE: Retinal pigment epithelium; ONL: Outer nuclear layer; INL: Inner nuclear layer; GCL: Ganglion cell layer. The bar represents 20 μm.

Figure 2 AT1-R activation by angiotensin II produced by the retina stimulates several pathways involved in the pathogenesis of DR such as inflammation, oxidative stress, leukostasis and angiogenesis. AT1-R:Angiotensin II type 1 receptor; AT2-R: Angiotensin II type 2 receptor; AGEs: Advanced glycated end products; BM: Basal membrane; BRB: Blood retinal barrier; ECM: Extracellular matrix; VEGF: Vascular endothelial growth factor.

Figure 3 SST immunofluorescence (red) in the human retina showing a higher expression in RPE than in the neuroretina from a human eye donor. RPE:Retinal pigment epithelium; ONL: Outer nuclear layer; INL: Inner nuclear layer; GCL:Ganglion cell layer.

Figure 4 Comparison of Epo (upper pannel, green) and EpoR (lower pannel, red) immunofluorescence in the human retina between representative samples. A, C: Non-diabetic donor; B, D: Diabetic donor. RPE: Retinal pigment epithelium; ONL: Outer nuclear layer; INL: Inner nuclear layer; GCL: Ganglion cell layer. The bar represents 20 mm.