Fig. 7From: FAF1 mediates necrosis through JNK1-mediated mitochondrial dysfunction leading to retinal degeneration in the ganglion cell layer upon ischemic insultFAF1 ablation protects retinal cells in ganglion cell layer (GCL) against retinal ischemic injury in mouse model (a) Schematic representation of the strategy used to target the exons encoding FAF1. A fusion neo cassette was used for positive selection. The EcoRV (EV) restriction endonucleases used for DNA digestion: wild-type, 9 kb; neo loxP-floxed, 7 kb. Triangles: loxP sites. b FAF1 expression levels were assessed via immunoblot analysis of protein lysates from retinas of Dkk3-Cre;Faf1+/+ and Dkk3-Cre;Faf1flox/flox mice. c Schematic diagram of the experimental design of the mouse model of retinal ischemia. The mice were sacrificed either 1 h or 3 days after induction of intraocular hypertension. d Left panel: immunoblot assay showing JNK1 activation in response to retinal ischemia in retinas of Dkk3-Cre;Faf1+/+ and Dkk3-Cre;Faf1flox/flox mice (n = 3 eyes). Right panel: immunoblot assay showing JNK1 activation in response to retinal ischemia in retinas of Dkk3-Cre;Faf1+/+ and Dkk3-Cre;Faf1flox/flox mice (n = 3 eyes). e The enucleated eyes were stained with HE. Histological images showing alterations in retinal morphology. INL, inner nuclear layer; ONL, outer nuclear layer. Scale bar = 20 μm. f The graph shows the number of cells in the GCL of the central region of the retina in HE-stained samples (n = 6 eyes). The data (d and f) are expressed as the mean ± S.E.M. of three independent experiments. Statistical comparisons were evaluated using ANOVA followed by Tukey’s HSD (d and f) post hoc analysis. ***P < 0.001, and **P < 0.01Back to article page