Fig. 3

Glutamate-driven astrocytic MAO-B leading to reactive astrogliosis and astrocytic scar formation. a Schematic representation of glutamate-driven astrocytic MAO-B inducing reactive astrogliosis and astrocytic scar formation. b-d Western blot analysis for EAAT1 and MAO-B expression in astrocyte monocultures upon glutamate treatment. Glutamate treatment increased MAO-B expression in astrocytes. Blockage of glutamate transport activity by using glutamate transporter inhibitor (TBOA) decreased MAO-B expression. e, f Reactivity of astrocyte monocultures upon glutamate treatment assessed by immunostaining with GFAP. Inhibiting glutamate transport (TBOA) or MAO-B (KDS2010) decreased GFAP expression. g ELISA for CSPGs deposited from reactive astrocytes. h, i Immunofluorescence images and quantification of GFAP intensity in the mouse tissues. j, k Immunofluorescence images and quantification of CSPGs intensity in the mouse tissues. Quantitative data were presented as means ± SD (n = 3, unless otherwise noted). *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001. p values were calculated by two-tailed unpaired Student's t-test for comparisons between two groups, and by one-way ANOVA for multiple comparisons. Scale bars represent 100 μm