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Fig. 1 | Journal of Neuroinflammation

Fig. 1

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

Fig. 1

Expression of C1q is present at normal levels in the brains of C1qa FL/FL mice but nearly absent in C1qa FL/FL :Cx3cr1 CreERT2 mice independent of tamoxifen administration. C1q staining in hippocampus of a WT, b C1qa FL/FL, and c C1qa FL/FL :Cx3cr1 CreERT2 mice and in the cortex of d WT, e C1qa FL/FL, and f C1qa FL/FL :Cx3cr1 CreERT2 in the absence of tamoxifen treatment. Representative images of n = 3–4 animals per genotype (ages 3–6 m) in (a–f). Scale bars: a–c:200 um, d–f: 50 um. g Representative western blots of total brain protein extract (60 ug per lane) from WT, C1qa FL/FL, and C1qa FL/FL:Cx3cr1 CreERT2, run under reducing conditions and probed with polyclonal anti-mouse C1q (1151) and anti-actin, as a loading control. h Densitometric ratio of C1q/ß-actin from several western blots performed as in (g), presented as the means +/− SEM of 4–5 animals per group as noted. *P < .03 relative to either WT or C1qFL/FL lacking Cre by one-way ANOVA followed by Bonferroni’s multiple comparisons test

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