Fig. 6
From: Intravitreal delivery of NMO-IgG causes primary retinal damage in the absence of optic nerve injury

Microglial C1q contributes to neuronal injury in NMO-IgG-induced RGC injury. a mRNA levels of C1q in retinas treated with NMO-IgG or HC-IgG (n = 4 per group). b Representative image of immunofluorescence staining showing C1q expression in microglia (Iba1+ cells) within the retina treated with NMO-IgG or HC-IgG (n = 4 per group). c Pie graph of the percentage of C1q+ microglia (n = 3 per group). d Bar graph showed the C1q+ microglia numbers in retina treated with NMO-IgG or HC-IgG (n = 3 per group). e Bar graph of C1q mRNA level in retina treated with normal diet or PLX3397 diet (n = 3 per group). f Bar graph of C3 mRNA level in retina treated with normal diet or PLX3397 diet (n = 3 per group). g PLX3397 inhibits NMO-IgG-induced C1q expression but did not change retina C3 expression in NMO-IgG treated retina (n = 3 per group). h Bar graph shows the C1q concentration in the culture medium of BV2 cells treated with mouse complement C3 (n = 4 per group). i CCK8 assay shows the cell viability of primary RGCs treated with PBS or C1q. C1q induced significant cell damage as measured by CCK8 assay (n = 4 per group). j ANX005 reduces C1q-induced RGCs injury in a dose-dependent manner (n = 4 per group). *p < 0.05, **p < 0.01, ***p < 0.001. t-test (a, c–g, i) or One-Way ANOVA (h, j)