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Fig. 7 | Cell Communication and Signaling

Fig. 7

From: FAF1 mediates necrosis through JNK1-mediated mitochondrial dysfunction leading to retinal degeneration in the ganglion cell layer upon ischemic insult

Fig. 7

FAF1 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 < 0.01

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