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Figure 4 | Journal of Neuroinflammation

Figure 4

From: Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis

Figure 4

Poly(ADP-ribose) polymerase 2 (PARP-2) contributes to macrophage accumulation and spinal demyelination in experimental autoimmune encephalomyelitis (EAE). CD11b immunofluorescence was used to detect macrophage/microglial cells activated by EAE. (B) Representative images illustrating elevated CD11b+ immunoreactivity in wild-type EAE spinal sections compared with sham sections (A). PARP-2 deletion reduced CD11b IR (C). Results were quantified in (D). Values are mean ± SEM (n = 3 to 7) and were analyzed using one-way analysis of variance (ANOVA) with the Student Newman-Keuls multiple comparison test. **P <0.01 compared to sham; ††P <0.01 compared to wild-type EAE; not significant = P >0.05. Scale bars are 200 μm (top row, A-C) and 25 μm (bottom row, (A-C)). Bottom row represents magnification of framed areas in the top row. Demyelination was assessed in peak disease EAE mice by staining with solochrome cyanin. Wild-type sham spinal cord white matter is thoroughly myelinated, as indicated by deep blue staining (E). Wild-type EAE spinal cords exhibit extensive areas of demyelination (F). EAE in PARP-2 null spinal cords produced only a low degree of demyelination (G) relative to wild-type controls. Results are quantified in (H) and show a significant reduction in demyelination of PARP-2 null cords compared to wild-type cords in EAE. Scale bars are 200 μm. Values are mean ± SEM (n = 3 to 6). Results in (H) were analyzed using non-parametric two-tailed Mann–Whitney test. *P <0.05 compared to wild-type EAE group.

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