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Fig. 8 | Molecular Neurodegeneration

Fig. 8

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

Fig. 8

C1q localisation in the mouse retina after photo-oxidative damage (PD) and in human AMD retinas. a No immunoreactivity to C1q or F4/80 was detected in retinas from dim-reared/control animals. b At 7 days of PD, C1q+ cells were detected in the subretinal space at the lesion site. c At 7 days of PD, F4/80+ cells were also detected at the lesion site. d Co-localisation of C1q and F4/80 was observed in cells in the subretinal space at the lesion site. e-g At the lesion edge C1q+/F4/80+ macrophages were present in the subretinal space. h Negative control slide for the mouse retinal immunohistochemistry showed no specific staining for either C1q or F4/80. i There was no immunoreactivity for C1q protein in the retina of C1qa−/− mice at 7 days after photo-oxidative damage. j C1q localisation in the normal human retina. No C1q-expressing cells were detected in the normal retina. k C1q immunoreactivity was detected adjacent to the subretinal drusen of early AMD retinas (arrows). l-n At the lesion edge, C1q-expressing cells were present in the subretinal space of AMD retina where IBA1+ cells were predominant (arrows). o C1q+ immunoreactivity co-localised in IBA1+ macrophages. p, q C1q+/IBA1+ cells at higher magnification. r Negative control slide for human AMD immunohistochemistry showed no specific staining for either C1q or IBA1. Representative images derived from N = 3 per group. INL, inner nuclear layer; ONL, outer nuclear layer; OS/IS, outer/inner segments. Scale bars represent 10 μm in O-Q; elsewhere 50 μm

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