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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: Caspase-7: a critical mediator of optic nerve injury-induced retinal ganglion cell death

Fig. 5

Protection by caspase-7 knockout against ON crush-induced RGC loss. a Representative retina cross-section images with RBPMS immunolabeling of WT and Casp7 −/− mice. Images of both ON crush (7 d and 28 d post injury) and uninjured control eyes are shown. GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. Scale bar = 100 μm. b Representative images showing RBPMS immunolabeled retinal flat-mounts of WT and Casp7 −/− mice. Images of both ON crush (7 d, 14 d, and 28 d post injury) and uninjured control eyes are shown. Scale bar = 100 μm. c Quantitation of RBPMS-positive RGCs in uninjured and ON crush flat-mounted retinas of WT and Casp7 −/− mice. There was no difference in RGC densities between uninjured eyes of WT and Casp7 −/− mice. ON crush caused a steady decline in the number of RGCs in WT retina in comparison to Casp7 −/− retina, which showed a significant preservation of RGCs. The values were represented as mean ± SD (n = 6). *: p < 0.05 versus the respective uninjured control group, #: p < 0.05 versus the “WT (ON crush)” group by One Way-ANOVA then Tukey–Kramer post hoc test

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