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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Deficiency of microglial Hv1 channel is associated with activation of autophagic pathway and ROS production in LPC-induced demyelination mouse model

Fig. 4

HV1 knockout inhibited autophagosomes in microglia and facilitated myelinated ultrastructure. a Western blot analysis of LC3 expression in the lesion of corpus callosum. b Quantification of the LC3 II/LC3 I was measured and calculated as fold change over contralateral. N = 6-8 mice for each group. c Western blot analysis of P62 and beclin-1 expression in the lesion of corpus callosum of 5 dpi. d Quantification of the P62 and beclin-1 was measured and calculated as fold change over contralateral. N = 8 mice for each group. e Representative images of Iba-1 and LC3B co-localization and P62 puncta in the CC of WT and Hv1−/− mice of 5 dpi (scale bar, 50 μm and 5 μm). f Quantification analysis of the ratio of LC3B+Iba-1+/Iba-1+. WT mice of 5 dpi. N = 6-8 mice; Hv1−/− mice, N = 5-9 mice. g Representative electron microscopy images for myelinated ultrastructure in the CC from different groups (scale bar, 2 μm). h Quantitative analysis of the ratio. N = 280 myelinated axons (70 axons per mouse, 4 mice per group) for each group. i Representative electron microscopy images showed the accumulation of autophagosomes in microglia in the CC at 10 dpi. Green arrows indicate autophagosomes (scale bar, 1 μm). Data are shown as mean ± SD, **P < 0.01, ***P < 0.001, two-way ANOVA with Dunnett’s post hoc test

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