Fig. 6: Nogo-A protein is increased in the vitreous and in the retina of patients affected by diabetic retinopathy.

a Western blot analysis was carried out to detect Nogo-A protein in the vitreous of donors. Anti-Nogo-A antibody allowed to detect recombinant human Nogo-A protein. b In the vitreous of non-diabetic patients, Nogo-A signal was very weak in comparison to patients with diabetes and proliferative diabetic retinopathy. c Immunofluorescent stainings in human retinal sections allowed to visualize Nogo-A in cell bodies (arrows) of the ganglion cell layer (GCL) and in Müller cell endfeet (EF). Dapi was used to recognize retinal cell layers in blue. To distinguish astrocytes from Müller cell processes in the nerve fiber layer (NFL), GFAP and GS were used respectively as specific cell markers. Without diabetes, astrocytes are the only glia expressing GFAP. They were deprived of Nogo-A staining. In contrast, Nogo-A was colocalized with GS in Müller cell endfeet. d In the retina of a diabetic patient, Nogo-A and GS were upregulated in Müller cells whose radial processes span the whole retinal thickness. e In the macula of a diabetic retinopathy (DR) patient, severe cystoid macular edema (CME) was observed. Around prominent cysts, Nogo-A and GFAP expression was strongly upregulated in gliotic Müller cells. These observations link Nogo-A expression increase with different stages of diabetic retinopathy. Scale bars = 20 μm.