Skip to main content
. 2017 Feb;187(2):352–365. doi: 10.1016/j.ajpath.2016.10.009

Figure 3.

Figure 3

CXCL10/CXCR3 pathway is activated in TON. Wild-type mice were subjected to traumatic optic neuropathy (TON). A: Quantitative PCR analysis of CXCL10 mRNA expression in noninjured retinas [control (Con)] or injured retinas at 3, 6, 12, and 24 hours after TON. B: Normal and TON-performed eyes were collected at 6 hours after TON. CXCL10 mRNA localization was assessed in retinal frozen sections by fluorescence in situ hybridization with RNAscope Fluorescent Multiplex Kit. Green fluorescent signal reflects CXCL10 mRNA expression, and DAPI (blue) stains nuclei. Arrows indicate CXCL10-expressing retinal cells in the ganglion cell layer (GCL). C: Enzyme-linked immunosorbent assay analysis of CXCL10 protein in control or TON-performed retinas at 6 hours after TON. D: Quantitative PCR analysis of CXCR3 mRNA expression in control or injured retinas at 3, 6, 12, and 24 hours after TON. E: Representative images of CXCR3 immunostaining in retinal frozen sections from control and TON-performed eyes at 24 hours after TON. Fluorescent signal (red) reflects CXCR3 staining. n = 4 to 5 mice (E). ∗P < 0.05, ∗∗P < 0.01 versus control. Scale bars = 50 μm (B and E). INL, inner nuclear layer; ONL, outer nuclear layer.