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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Cell-specific deletion of C1qa identifies microglia as the dominant source of C1q in mouse brain

Fig. 5

C1q reactivity in the hippocampus is nearly absent in AD C1qa FL/FL mouse models crossed to C1qa FL/FL:Cx3cr1 CreERT2 mice. a, b C1q immunostaining (red) in the brains of C1qa FL/FL (left column) and Arctic C1qa FL/FL (right column) without (top row) or with Cx3cr1 CreERT2 (bottom row) at 5 (a) and 10 m (b) of age. Representative images of the molecular layer of 8–10 animals per genotype per age. Acquisition time and camera gain are identical for each panel within (a or b). The exposure time was shorter in (b) than in (a) to avoid overexposure due to higher levels of C1q in the Arctic brain at 10 months than at 5 months of age (c and d). Scale bars: 50 um. Western blot analysis for C1q in hippocampal extracts (60 ug per lane) from C1qa FL/FL, Arctic:C1qa FL/FL, C1qa FL/FL:Cx3cr1 CreERT2 and Arctic:C1qa FL/FL:Cx3cr1 CreERT2 at c 5 and d 10 months of age. Representative of 4 animals per genotype per age. e, f Increased C1qa mRNA expression relative to Hprt in hippocampal extracts from Arctic compared C1qa FL/FL, mice at both e 5 months and f 10 months, with almost complete absence in all animals containing C1qa FL/FL:Cx3cr1 CreERT2. Representative of 2–4 animals per genotype for 5mo and 3 animals per genotype for 10mo old mice. g Quantification (% Field Area) of amyloid and h CD45 staining in Arctic C1qa FL/FL with and without Cx3cr1CreERT2 at 5 (left) and 10 (right) months of age. n = 8–10 mice per genotype per age. Not statistically different by genotype at each age as assessed by one-way ANOVA (CD45 p = 0.10 (5 months) and p = 0.9 (10 months); Aß p = 0.8 (5 months) and p = 0.95 (10 months)

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