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Fig. 3 | Journal of Neuroinflammation

Fig. 3

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

Fig. 3

Tamoxifen treatment of C1qa FL/FL :Thy1 CreERT2 mice did not change levels of C1q in the brain. C1q reactivity (red) in hippocampus of untreated (UT) WT (a) and C1qa FL/FL :Thy1 CreERT2 (b–f) mice treated with vehicle (b, c) or tamoxifen (d, e, f) for 5 days and perfused at 3,7,or 14 days after treatment. Age 5 m. Scale bar: 50 μm in (a); same magnification in (a–f). Mean intensity of C1q immunofluorescence (g) in the molecular layer of hippocampus of pictures shown in panels in (a–f). Brain extracts (60 ug per lane) (h) from C1qa FL/FL:Thy1 CreERT2 treated with vehicle (V) or tamoxifen (T) as in (a–f), C1q WT at 5 m, and wild type (WT) plasma (1 ul), were run under reducing conditions and probed with polyclonal anti-C1q (1151) and anti actin, as a loading control. Densitometric ratio (i) of C1q/ß-actin of blot in (h)

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