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. 2021 Jan 1;18(4):964–974. doi: 10.7150/ijms.49460

Figure 1.

Figure 1

CX3CL1 induced proliferation and promoted migration in HUVECs. HUVECs after serum starvation (DMEM+0.5% FBS) for 48 hours were transfected with si-control (si-NC) or si-CX3CL1 for 48 hours. 8-week-old male mice were fed a high fat-, high cholesterol diet (40% fat (20%w), 1.25% cholesterol for eight weeks. A: Cell proliferation was measured by counting cell numbers as described in “Experimental Procedures.” n=3. Data are expressed as mean±S.D (**P< 0.01). B and C: Cell proliferation was measured by EdU assay. n=3. Data are expressed as mean±S.D (**P< 0.01). D and E: The effect of overexpressed or knocked down CX3CL1 on HUVECs migration of was detected by Wound-healing assay. (**P< 0.01). The transwell assay was also used to detect the migration-stimulating effects of overexpressed or knocked down CX3CL1 on HUVECs. The number of cells migrated to the lower side of the transwell chambers was counted and photographed in five fields (the upper, the lower, the left, the right, and the middle) of three independent experiments, and the migration capacity was calculated by SPSS statistical soft. (**P< 0.01). F. The effect of atherosclerosis on the expression of VEGFA and CX3CL1 was examined by ELISA assay in ApoE-/- mice. (**P< 0.01)