Figure 3.
Figure 3. Effect of Mer inhibition on ICAM-1 and VCAM-1 upregulation induced by exogenous Gas6 or the exposure of sera isolated from patients with grade III aGVHD in ECs. (A,D) The expression of ICAM-1 and VCAM-1 in ECs was upregulated by exogenous Gas6. The ECs were incubated for 24 hours with exogenous Gas6 (0, 100, 200, 400 ng/mL), followed by western blotting. Representative data are from 4 independent experiments. *P < .05. (B,E) The expression levels of ICAM-1 and VCAM-1 were increased by exogenous Gas6, and 5 μmol/L UNC2250, a selective Mer tyrosine kinase inhibitor significantly suppressed ICAM-1 and VCAM-1 upregulation in the ECs, which were then incubated for 24 hours with exogenous Gas6 (100 ng/mL) with or without UNC2250 (5 μmol/L), followed by western blotting. Results are shown as mean ± SD of statistical analyses from 4 separate experiments. *P < .05. (C,F) The expression of ICAM-1 and VCAM-1 was significantly increased by the exposure of sera isolated from patients with grade III aGVHD, and 5 μmol/L UNC2250 suppressed the ICAM-1 and VCAM-1 upregulation in ECs. The ECs were incubated for 24 hours with the sera isolated from patients with or without grade III aGVHD at a level of 50 (vol/vol) of the total medium with or without UNC2250 (5 μmol/L), followed by western blotting. Results are shown as mean ± SD of statistical analyses from 4 separate experiments. *P < .05. (Ga-c) The effects of GVHD sera on the phosphorylation of Mer, Axl, and Tyro3 in the ECs. Thirty minutes of incubation of GVHD sera specifically induced the phosphorylation of Mer in the ECs. Representative data are from 3 independent experiments.

Effect of Mer inhibition on ICAM-1 and VCAM-1 upregulation induced by exogenous Gas6 or the exposure of sera isolated from patients with grade III aGVHD in ECs. (A,D) The expression of ICAM-1 and VCAM-1 in ECs was upregulated by exogenous Gas6. The ECs were incubated for 24 hours with exogenous Gas6 (0, 100, 200, 400 ng/mL), followed by western blotting. Representative data are from 4 independent experiments. *P < .05. (B,E) The expression levels of ICAM-1 and VCAM-1 were increased by exogenous Gas6, and 5 μmol/L UNC2250, a selective Mer tyrosine kinase inhibitor significantly suppressed ICAM-1 and VCAM-1 upregulation in the ECs, which were then incubated for 24 hours with exogenous Gas6 (100 ng/mL) with or without UNC2250 (5 μmol/L), followed by western blotting. Results are shown as mean ± SD of statistical analyses from 4 separate experiments. *P < .05. (C,F) The expression of ICAM-1 and VCAM-1 was significantly increased by the exposure of sera isolated from patients with grade III aGVHD, and 5 μmol/L UNC2250 suppressed the ICAM-1 and VCAM-1 upregulation in ECs. The ECs were incubated for 24 hours with the sera isolated from patients with or without grade III aGVHD at a level of 50 (vol/vol) of the total medium with or without UNC2250 (5 μmol/L), followed by western blotting. Results are shown as mean ± SD of statistical analyses from 4 separate experiments. *P < .05. (Ga-c) The effects of GVHD sera on the phosphorylation of Mer, Axl, and Tyro3 in the ECs. Thirty minutes of incubation of GVHD sera specifically induced the phosphorylation of Mer in the ECs. Representative data are from 3 independent experiments.

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