2013, Number 5
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Ann Hepatol 2013; 12 (5)
Notch signal protects non-parenchymal cells from ischemia/ reperfusion injury in vitro by repressing ROS
Heng-Chao Y, Lu B, Shu-Qiang Y, De-Sheng W, Lin W, Hua H, Ke-Feng D
Language: English
References: 26
Page: 815-821
PDF size: 436.11 Kb.
ABSTRACT
Background. We have previously reported that Notch signaling pathway protects hepatocytes from ischemia/
reperfusion (I/R) injury by repressing reactive oxygen species (ROS) production. However, apart from
hepatocytes, non-parenchymal cells including vascular endothelia cells, Kupffer cells and hepatic stellate
cells are also reported to be involved in hepatic I/R injury.
Aim. To clarify the role of Notch signaling in
non-parenchymal cells subjected to I/R injury.
Materials and methods. Human Umbilical Vein Endothelial
Cells (HUVECs), mouse macrophage line RAW264.7 and rat hepatic stellate cell line HSC-T6 were cultured
and subjected to I/R injury, respectively. Activation of Notch signaling was assessed by NICD western blot.
Then, pharmacological inhibitor (γ-secretase inhibitor GSI) was used to block Notch signaling of related
cell lines in vitro. Intracellular ROS was detected and analyzed by FACS and apoptosis was examined by TUNEL
staining and Annexin V staining.
Results. Notch signaling responded to I/R injury and I/R injury induced
activation of Notch signaling in nonparenchymal cells. Notch signal deficiency led to overproduction
of ROS and aggravated cell death of non-parenchymal cells subjected to I/R injury.
Conclusion. Notch signal
protectes non-parenchymal cells from I/R injury by repressing ROS.
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