Research Paper Advance Articles

Loss of β-catenin via activated GSK3β causes diabetic retinal neurodegeneration by instigating a vicious cycle of oxidative stress-driven mitochondrial impairment

Figure 5. Knock-down of β-catenin abrogated the protective effect of GSK3β depletion on HFD-induced diabetic retinal neurodegeneration. A Cy5-labeled si-β-catenin was intravitreally co-injected with si-GSK3β into the right eye of HFD-induced diabetic mice (HFD+si- GSK3β/R-si-β-catenin), while scramble si-sc was co-administrated with si-GSK3β in the contralateral left eye as a control (HFD+si-GSK3β/L-si-sc). (A) Representative immunofluorescence for active β-catenin (green, active β-catenin; red, Cy5; blue, DAPI; scale bar, 100 μm). Areas boxed in are shown at higher magnification. (B) Western blotting for GSK3β and active β-catenin. Relative intensities were quantified. (C) Representative retinal immunofluorescence staining for synaptophysin (green; scale bar, 100 μm). Areas boxed in are shown at higher magnification. (D) Representative SEM of retinal sections. Areas boxed are shown at higher magnification. Scale bar, 10 μm. (E) Representative waveforms of VEP and quantification of differences in peak amplitude (N1-P1). Data are means ± SEM. n = 4 eyes per group. **P < 0.01 vs contralateral eye injected with scramble si-sc. See also Supplementary Figures 2E, 3E and 4C.