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. 2019 Aug 19;15(10):2240–2255. doi: 10.7150/ijbs.35356

Figure 1.

Figure 1

Irradiated HaCaT cells cause slower migration of unirradiated WS1 fibroblasts after co-culture, which involves reactive oxygen species (ROS). (A) The cell proliferation of unirradiated bystander WS1 cells was not inhibited after co-culture with α-irradiated (left panel) and X-irradiated (right panel) HaCaT cells. (B) The representative images of the wound scratches of WS1 cells after co-culture with irradiated HaCaT cells. (C) The quantification of the area of the wound scratches of bystander WS1 cells after co-culture with α-irradiated (left panel) and X-irradiated (right panel) HaCaT cells, showing slowed migration of bystander WS1 cells after co-culture with irradiated HaCaT cells. (D) The elevation of the intracellular ROS levels of bystander WS1 cells after co-culture with irradiated HaCaT cells for 1 h, as well as the effect of NAC on the elevation. (E) The quantification of the area of the wound scratches of bystander WS1 cells after co-culture with α-irradiated (left panel) and X-irradiated (right panel) HaCaT cells in the presence of NAC, showing that NAC almost abolished the slowed migration of bystander WS1 cells after co-culture with irradiated HaCaT cells. All the data represent the means ± SEM from three independent experiments (n=3). *P<0.05, **P<0.01 and ***P<0.001 compared with the relative control.