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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: Subretinal macrophages produce classical complement activator C1q leading to the progression of focal retinal degeneration

Fig. 2

Retinal morphology and measures of inflammation in C1qa−/− retinas at 7 days of photo-oxidative damage (PD) (a). b-c Photoreceptor cell death indicated using TUNEL at the focal lesion site in wild-type (WT) and C1qa−/− retinas. d-f Quantitative analyses showed no significant difference between C1qa−/− retinas and WT retinas in the total numbers of TUNEL+ cells (d), thickness of the outer nuclear layer (ONL) at the lesion site (e), or in adjacent retina (f) (NS, P > 0.05). g-i The IBA1+ cells were shown in amoeboid morphology in the outer retina in WT and C1qa−/− retinas (arrows, g, h). There was no remarkable difference in the numbers of IBA1+ cells present after 7 days of PD (i) (NS, P > 0.05). j-k Abundance of C3d proteins by Western blotting appeared comparable in the two groups (j), and confirmed by optical densitometry (k). l-n No significant differences in retinal function were detected in C1qa−/− compared to WT at 7 days of PD. o Expression of classical complement genes C2, C4a, and Serping1 significantly reduced in C1qa−/− retinas compared to WT (P < 0.05), whereas the Cfh of the alternative pathway displayed a significant upregulation (P < 0.05), but had no significant change in Cfb (P > 0.05). Student t-test, one- and two-way ANOVA followed by post-hoc multiple comparison were used for analysis (N = 6 per group, *represent P < 0.05; NS represents no significance). For representative images, scale bars represent 50 μm

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