Endothelial Shp2 deficiency controls alternative activation of macrophage preventing radiation-induced lung injury through Notch signaling

Published: 18 January 2022| Version 2 | DOI: 10.17632/bsdc4jmhwm.2
Contributor:
Xue Zhang

Description

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.

Files

Steps to reproduce

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.

Institutions

Zhejiang University School of Medicine

Categories

Cell Communication, Mouse Model

License