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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: GSK3β-mediated tau hyperphosphorylation triggers diabetic retinal neurodegeneration by disrupting synaptic and mitochondrial functions

Fig. 2

HFD promotes hyperphosphorylation of tau in neural retina and optic nerves. (a) Representative images of retinal double immunostaining for phospho-tau (pS396- or pT231-Tau; green) with total-tau (Tau-5; red), and non-phospho-tau (Tau-1; green) with Tau-5 (red) from mice fed with RD or HFD for 16, 20 and 24 weeks, respectively. Nuclei were counterstained with DAPI. Scale bar, 100 μm. (b) Representative images of double immunostaining for phospho-tau (pS396- or pT231-Tau; green) with total-tau (Tau-5; red) of RGCs axons at the proximal portions of optic nerves in longitudinal sections of optic nerves from mice fed with RD or HFD for 16 weeks. Scale bar, 20 μm. Higher magnifications (scale bar, 5 μm) are shown in the boxed lower panels, respectively. (c) Western blot analyses of pS396-Tau, pS404-Tau, pT231-Tau, pT205-Tau, Tau-1 and Tau-5 in total retina lysate. Intensities were quantified and normalized against the level of GAPDH and expressed as fold changes of protein abundance in the retina from HFD groups relative to their age-matched controls. Data are means ± SEM. n = 6 (a, b) or n = 4 mice (b) per group. *P < 0.05 and **P < 0.01 vs age-match RD controls. NS, no significant difference. OPL, outer plexiform layer

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