Fig. 8

TNFα treatment results in significantly enhanced HSC homing and engraftment. a Mean fluorescence intensity (MFI) of surface CXCR4 in vehicle, TNFα (TNF, 100 ng/mL), Andrographolide (Andro)-, TNF + Andro-, BMS345541 (BMS)-, TNF + BMS-treated human CB CD34⁺ cells, as assessed by flow cytometry. None indicates the group without any treatment. Data pooled from three independent experiments are shown (n = 6, one-way ANOVA, ***p < 0.001). b The cells were cultured in the presence of vehicle or TNFα (TNF, 100 ng/mL) for 16 h and then allowed to migrate toward the indicated concentrations of SDF-1 for 4 h. Vehicle or TNF-treated human CB CD34⁺ cells migration in the presence of the CXCR4 antagonist, AMD3100 (5 μg/mL) were also shown. Data pooled from three independent experiments are shown (n = 3, one-way ANOVA, ***p < 0.001). c The percentage of human CD45⁺ cells in the BM of NSG mice 24 h after transplantation with 500,000 CB CD34⁺ cells that had been treated with vehicle, Andrographolide (Andro, 10 μM), TNFα (TNF, 100 ng/mL), or TNF + Andro. Data pooled from four independent experiments are shown (n = 4 mice per group, one-way ANOVA, **p < 0.01, ***p < 0.001). d Representative flow cytometric analysis of human engraftment in the BM of NSG mice transplanted with human CB CD34⁺ cells treated with vehicle control or TNFα (TNF, 100 ng/mL) for 16 h. Human engraftment was assessed as the percentage of human CD45⁺ cells. e The percentage of human CD45⁺ cells, B-cell (CD19⁺), and myeloid cell (CD33⁺) chimerism in the BM of NSG mice after transplantation with 10,000 CB CD34⁺ cells that had been treated with vehicle or TNFα (TNF, 100 ng/mL), n = 5 mice per group, t-test, *p < 0.05. For all panels, data are shown as dot plots (mean ± SEM)