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. 2020 Nov 22;25(1):434–447. doi: 10.1111/jcmm.16098

Figure 4.

Figure 4

(A‐C) MaR1 increased Aβ42‐uptake in d‐THP‐1 cells. Differentiated THP‐1 (d‐THP‐1) cells were incubated for 20 min with 1 μg/mL HiLyteFluor 488‐conjugated Aβ42 alone together with 5 μM MaR1. Incubation with vehicle served as control. Aβ42 uptake was observed by fluorescence microscopy (A) and assessed by flow cytometry (B and C). Green fluorescence can be seen inside the cells indicating the uptake of Aβ42 (A). (B) shows an example of flow cytometry data from one experiment. For each treatment, one thousand gated events were analysed in the FITC‐channel. Vehicle control (black line) was considered as Aβ42‐negative. A right shift of the peak was observed upon incubation with Aβ42 indicating Aβ42‐uptake (red line), and MaR1 treatment further increased the Aβ42‐uptake (green line). Analysis of the data from ten experiments showed that MaR1 significantly increased the Aβ42‐uptake in d‐THP‐1 cells (C). Analysis of variance (ANOVA) was performed with the non‐parametric Kruskal–Wallis (K‐W) test, using the built‐in post hoc test for multiple comparisons to find significant differences between treatments. *P < 0.05 vs. 1 μg/mL Aβ42. Aβ = β‐amyloid; FITC = fluorescein isothiocyanate; MaR1 = maresin 1