Endothelial Shp2 deficiency controls alternative activation of macrophage preventing radiation-induced lung injury through Notch signaling
Our findings demonstrate that endothelial Shp2 is a key regulator in radiation-induced lung injury by maintaining the radiation-induced Jag1 level through the β-catenin pathway, thereby reducing alternative macrophage activation to relieve radiation-induced lung injury. Two short-term and a long-term mouse model were used to evaluate the role of endothelial Shp2 in radiation-induced lung injury. The in vitro co-culture system was used to investigate the relationship between irradiated-endothelium and macrophage. HUVECs and MLECs were used here for in vitro study.
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Western blotting, qRT-PCR, immunofluorescence staining, Elisa were the main experimental technology here. Every experiments were be repeated at least three times. Results were be measured by ImageJ or Graphpad.