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. 2020 Aug 6;11:1258. doi: 10.3389/fimmu.2020.01258

Figure 4.

Figure 4

S100A8 and S100A9 trigger apoptotic effects on EoL-1-IR cells. (A) EoL-1 and EoL-1-IR cells were incubated for 24, 48, and 72 h in the absence (Con) or presence of imatinib at the indicated concentration. Apoptosis was analyzed by measuring the binding of annexin V-FITC and PI. (B) EoL-1 and EoL-1-1R cells were incubated for 72 h in the absence or presence of imatinib at the indicated concentration. Following cell lysis, phosphorylation and non-phosphorylation of PDGFRα, STAT3, AKT, ERK1/2, p38 MAPK, and JNK in the lysates were detected by Western blotting. (C,D) EoL-1 and EoL-1-IR cells were incubated for 24, 48, and 72 h in the absence (Con) or presence of indicated concentrations of S100A8, S100A9 (C), LPS (100 ng/mL) and MPLA (100 ng/mL) (D) (n = 3). Apoptosis was analyzed by measuring the binding of annexin V-FITC and PI. (E,F) EoL-1-IR cells were incubated for 24, 48, and 72 h in the absence (Con) or presence of S100A8 and S100A9 (10 μg/mL), and TLR4 expression was detected using Western blotting (E) and flow cytometry (F). Data are expressed as the means ± SD. *p < 0.05 and **p < 0.01 indicate a significant difference between the control and stimulator-treated groups. (G,H) EoL-1 cells were incubated with S100A8 and S100A9 (10 μg/mL) for 72 h. After cell lysis, the indicated protein expression in the lysates was detected by Western blotting. β-actin was used as an internal control.