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Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: Flow-cytometric microglial sorting coupled with quantitative proteomics identifies moesin as a highly-abundant microglial protein with relevance to Alzheimer’s disease

Fig. 4

Moesin knockdown impacts Aβ phagocytosis and pro-inflammatory cytokine production by microglia. a Overview of in-vitro knockdown studies in primary mouse microglia treated with Msn siRNA or sham siRNA under resting and LPS-stimulated conditions. b Results from qRT-PCR experiments demonstrating efficiency of Msn knockdown by siRNA as compared to sham siRNA. Y-axis represents relative mRNA expression (2-ΔΔCt method) normalized to Gapdh as housekeeping gene (three independent biological replicate experiments were performed per condition). c In-vitro phagocytic capacity of primary microglia for fAβ42 HiLyte488 following exposure to sham siRNA or Msn siRNA under resting and LPS-stimulated conditions. Phagocytic uptake of fAβ42 was measured as proportion of CD45+ microglia using untreated microglia as negative controls. For each sample, at least 2000 live CD45+ microglial events were captured. N = 3 independently performed biological replicate experiments. d-i Bar graphs displaying cytokine/chemokine data, shown as fluorescence intensity in arbitrary units (A.U.), obtained from microglial culture supernatants after siRNA sham or siRNA Msn treatment under resting and LPS-stimulated conditions: d IL10, e IL6, f TNF, g G-CSF, h CXCL10, i CCL3. Error bars represent ± SEM. Unpaired t-test: *p < 0.05, ***p < 0.0001

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