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. 2023 May 30;18(5):e0285597. doi: 10.1371/journal.pone.0285597

Fig 4. AM-mediated proliferation is not enhanced upon treatment with CCX771 or shRNA-mediated knockdown of ACKR3.

Fig 4

(A) Titration of AM in a LEC proliferation assay. Data from one out of two similar titration assays, performed with ndLECs and adLECs with 10 technical replicates per condition, are shown. (B) Treatment with CCX771 does not affect baseline proliferation of ndLECs. (C) CCX771 treatment does not alter AM-induced proliferation of primary human ndLECs. Data of three experiments with 10 technical replicates are shown in (B,C) and represented as mean ±SD. RM One-way ANOVA, Šídák’s multiple comparison test. (D) shRNA-mediated knockdown of ACKR3 does not alter proliferation induced by either 0.1nM, 1nM and 10nM AM in adLECs. Data of one out of one or two similar experiments with 10 technical replicates per condition are shown. (E) Data from (D) are shown as percentage of proliferation induced when compared to the corresponding untreated control. (F, G) Proliferation induced by 1nM AM was investigated in shRNA-transduced jdLECs. Data of three experiments are shown and represented as mean ±SD. Each data point represents the mean of 8 technical replicates, showing (F) Absolute fluorescence units as a readout of proliferation or (G) Percentage of proliferation induction relative to the untreated control. Statistics: Two-way ANOVA, Šídák’s multiple comparison test (D,E). RM-Two-way ANOVA, Šídák’s multiple comparison test (F,G). A p-value of p≥0.05 was considered not significant (ns).