Figure 4.

tRF-3001a regulates diabetes-induced retinal neuronal dysfunction in vivo

(A) Electrophysiology was performed to detect retinal neuronal function in non-diabetic mice (Ctrl), STZ-induced diabetic mice injected with negative control (NC) agomir, tRF-3001a agomir, NC antagomir, and tRF-3001a antagomir following 2-, 4-, or 6-month diabetes induction. The representative images were shown at 4 months after diabetes induction (n = 6). The amplitudes and latency of b waves were statistically calculated (n = 6).

(B and C) Immunofluorescence and quantitative analysis of GFAP staining (B) or GS staining (C) were conducted to detect retinal reactive gliosis along with the representative images (n = 6). Scale bar, 50 μm.

(D and E) Immunofluorescence and quantitative analysis of NeuN staining (D) or TUJ1 staining (E) were conducted to detect RGC survival. The representative images are shown (n = 6). Scale bar, 50 μm.

(F) Retinal whole mounts following TUJ1 staining were observed from the peripheral area. RGC survival rate was calculated by dividing the average number of TUJ1-positive cells in one field in the injured retina by that in the uninjured (Ctrl) retina (n = 6). Scale bar, 20 μm ∗p < 0.05 versus Ctrl; ^#p < 0.05 between the marked groups. The significant difference was evaluated by one-way ANOVA followed by post hoc Bonferroni test. See also Figures S6, S7, and S8.