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. 2013 Jan 2;123(2):646–656. doi: 10.1172/JCI64811

Figure 1. Relative hypodeimination in the RGC layer in demyelinating diseases.

Figure 1

(A–M) Immunofluorescence analyses to determine deimination levels. (A and B) Representative normal and MS brains (cerebral cortex; each from a 76-year-old male of mixed European descent) subjected to monoxime treatment, using an anti–citrulline-monoxime adduct antibody (green); (C and D) representative normal and MS human retinas treated as in A. Thin and thick arrows indicate normal and hyperdeimination, respectively. Scale bars: 100 μm (A–D). (E) Retinal sections from normal 5-month-old control mice and (F) transgenic ND4 mice treated as in A. Yellow thin arrows (E) indicate a subset of RGCs that is deiminated (green). Fluorescent spots (box and inset) are absent in ND4 mice (F). (G and H) Controls without monoxime treatment subjected to anti–citrulline-monoxime adduct immunofluorescence. Blue arrows (F) indicate hyperdeiminated regions. Arrowheads show nuclei stained with DAPI (blue). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer; PR, photoreceptor layer. Scale bars: 50 μm; 15 μm (inset) (E–H). (I and J) Sections of control (CD1) and ND4 mice brain (5 month old) treated as in A. (K) Citrullinated RGC numbers in 0.1 sq. mm of human retina from 5 control and 5 MS eyes (3 regions for each eye). (L) Thy1 and MAP 2 marker intensity in equal areas in GCL in control and ND4 mouse at 5 months of age. (M) The anti-citrulline–positive to Thy1-positive RGC cell ratio in the retina at indicated ages of ND4 and control mice (3 animals each) from equivalent regions of retina. *P < 0.05.