Fig. 1
The administration of anti-β1 integrin antibody to injured spinal cord in the sub-acute phase suppressed the glial scar formation in the chronic phase, leading to changes in the microglial distribution within the glial scar. a Time schedule of our in vivo experiments. Injured mice were intralesionally administered anti-β1 integrin antibody or control antibody at 9, 11, and 13 days post-injury (dpi). At 42 dpi, the injured spinal cord was analyzed. b Sagittal sections of the chronically injured spinal cords. Magnification of the inset is shown in the right figure. Asterisk indicates the lesion epicenter. GFAP, red; ColIαI, green. Scale bars, 250 μm on the left and 100 μm on the right. c Time course of the Basso Mouse Scale score after SCI. Error bar indicates mean ± SEM. Star indicates statistical significance (p < 0.05). A two-way repeated-measures ANOVA with the Tukey-Kramer post hoc test. n = 14 mice per group. d Peri-lesional glial scar of the chronically injured spinal cord. Microglia are mainly the lesion epicenter. β1Ab administration changed the microglial distribution within glial scars. Asterisk indicates the lesion epicenter. GFAP, red, TMEM119, white. Scale bar, 200 μm. e Gating strategy of fluorescence-activated cell sorting for selective isolation of microglia from injured spinal cord. Red-boxed population, Gr-1nega-int/CD11bhigh/CD45int, indicates microglial population. f The number of resident microglia in the injured spinal cord counted by FACS. Error bar indicates mean ± SEM. n.s. indicates not significant. Wilcoxon’s rank-sum test. n = 3 per each group, triplicate. F = 0.266