Fig. 8
From: NG2 glia regulate brain innate immunity via TGF-β2/TGFBR2 axis
NG2 glia deficiency contributes to neurodegeneration in both patients with Parkinson’s disease and MPTP-induced mouse PD model. a–c Downregulation of PDGFRα and CX3CR1 expression in the substantia nigra of patients with PD compared with control subjects. Student’s t test (n = 3). d–f Ablation of NG2 glia exacerbates microglial activation and nigral dopaminergic neuron loss elicited by MPTP treatment. d, e Downregulation of microglia CX3CR1 in the striatum of MPTP-induced PD model as revealed by qPCR analysis (d) or immunoblotting analysis (e). The mice were sacrificed 24 h following MPTP exposure (n = 3 per group). f Representative graph showing the mRNA levels of pro-inflammatory mediators and TGFBR1-3 in the CD11b-positive microglia isolated from the striatum of MPTP-induced PD model using MACS. Student’s t test, paired, (n = 6). *P < 0.05, ***P < 0.001. g–l Ablation of NG2 glia exacerbates microglial activation and nigral dopaminergic neuron loss elicited by MPTP treatment. g Schematic representation of the generation of DTRNG2 Tg mice and MPTP-induced PD mouse model. DT (300 ng/day) was given twice a day for 3.5 days. MPTP was given at 20 mg/kg for four times with 2-h intervals following NG2 glia ablation. h Immunofluorescent histochemical analysis of the ventral midbrain sections taken 7 days from DTROlig1 mice and littermate control that were challenged with MPTP. i–l Quantitative data shown in h. Two-way ANOVA with Bonferroni’s post test; (n = 3–6). *P < 0.05, **P < 0.01; ****P < 0.0001, ****P < 0.0001. Scale bars, 200 μm; scale bar in the inserts, 50 μm