Figure 3
Protein expression of endothelin-1 (EDN1) and endothelin receptor type B (EDNRB) in retinal tissue. (a) The retina of non-treated wild-type (labeled ‘‘W’’), NMDA-injected (control, labeled ‘‘C’’), or NMDA-injected-KUS121-treated mice (labeled ‘‘K’’) was analyzed by western blotting using an anti-EDN1 antibody. Actin was used as a loading control. Complete scans of western blots are shown in Supplementary Fig. S2a. (b) Comparison of EDN1 expression shown as ratios to actin (n = 5, for all treatments). **p < 0.01, vs. W, Tukey’s HSD. (c–f) Vertical sections of non-treated wild-type, NMDA-injected, NMDA-injected-KUS121-treated and NMDA-injected-KUS187-treated mice retinae were stained with an anti-EDN1 antibody or anti-EDNRB antibody. (c,d) Staining intensities of RGC layers with anti-EDN1 (c) or anti-EDNRB (d) antibody. The staining intensity of the RGC layer at distances of 400–800 μm from the optic nerve head was analyzed using BZ II Analyzer software. W: non-treated wild-type, C: NMDA-injected, K121: NMDA-injected-KUS121-treated, K187: NMDA-injected-KUS187-treated. (n = 3, for C and K121, n = 2, for W and K187) NS no significant difference compared with W, Tukey’s HSD. (e,f) Vertical sections of non-treated wild-type (WT), NMDA-injected (control), NMDA-injected-KUS121-treated (K121) and NMDA-injected-KUS187-treated mice (K187) retinae. The black bar represents 100 µm. GCL ganglion cell layer, IPL inner plexiform layer.
