Figure 1

Deletion of poly(ADP-ribose) polymerase 2 (PARP-2) protects neurological function and blood-spine barrier integrity in experimental autoimmune encephalomyelitis (EAE) mice. (A) PARP-2 null and littermate C57Bl/6 mice were immunized with myelin oligodendrocyte glycoprotein (MOG)_35–55 and neurological signs of EAE were scored for 35 days. (A) Daily neurological scoring profile for wild-type and PARP-2 null EAE mice. (B) Total disease burden (summed score/35 days) and peak neurological score were significantly reduced by PARP-2 deletion. (C) The number of days required to reach first peak disease score was significantly increased by PARP-2 deletion. (D) Spinal:serum fluorescence was measured following sodium fluorescein (Na-Fluor) administration intraperitoneally just prior to peak disease neurological score. The magnitude of the EAE-induced ratio increase was significantly less in PARP-2 mice than in wild-type animals. Values are expressed as mean ± SEM (n = 6 to 9). (B,C) *P <0.05, using non-parametric two-tailed Mann–Whitney test. (D) ***P <0.001 compared to respective sham control, †P <0.001 as indicated using one-way analysis of variance (ANOVA) followed by Student Newman-Keuls multiple comparisons test.