Fig. 5
From: The anti-inflammatory Annexin A1 induces the clearance and degradation of the amyloid-β peptide
ANXA1 increases microglial phagocytosis of Aβ1–42. a–b Phagocytosis of 5-FAM-labelled-Aβ1–42 or 5-FAM-labelled-scrambled Aβ1–42 by BV2 microglia incubated for 3 h with 3 μg/ml of these compounds in medium that has been conditioned by BV2 cells for 18 h overnight or freshly changed prior to Aβ incubation (n = 9), measured by FACS. b Phagocytosis of 5-FAM-labelled-Aβ1–42 (3 μg/ml) by BV2 microglia after 3-h incubation with anti-ANXA1-antibody (20 ng/ml) or anti-IgG-antibody when medium has been conditioned by BV2 cells overnight, measured by FACS (n = 9). c Phagocytosis of 5-FAM-labelled-Aβ1–42 (5 μg/ml) incubated for 3 h with BV2 microglia (untransfected, control shRNA or ANXA1 shRNA transfected) in the absence or presence of hrANXA1 (5 μg/ml) and/or selective FPR2 antagonist WRW4 (5 μM) (n = 3–9). d–f Quantification of mRNA levels of receptors involved in receptor-mediated endocytosis in BV2 cells treated with 3 μM Aβ1–42 with or without 5 μg/ml hrANXA1 for 16 h. d RAGE (n = 6 samples). e MARCO (n = 6). f FPR rs1 (n = 6). Values shown in graphs represent the mean value ± SEM and are expressed as a percentage change in comparison to the normalized control or fold change of control. Statistical analysis included Student’s independent two-tailed t test, one-way ANOVA with Bonferroni’s multiple-comparison post-test or two-way ANOVA with Bonferroni’s multiple-comparison post-test as appropriate. *p < 0.05, **p < 0.01, ***p < 0.001, ****/§§§§ p < 0.0001