Abstract
Accumulating evidence indicates that factor associated with suicide ligand (FasL) is a bidirectional regulator. At higher dosage, soluble FasL induced the apoptosis of Fas-expressing brain endothelial cells. Reduced concentration of soluble FasL (sFasL), however, promoted the proliferation and migration of brain endothelial cells. The effect of sFasL on endothelial cells proliferation was completely abolished by silencing Fas expression using siRNA. Treating brain endothelial cells with low-dose sFasL led to increased secretion of VEGF and up-regulated expression of FLIP, TRAF, and NF-κB that played a crucial role in the proliferation of endothelial cells. Our results further underscore the potential stimulating role of Fas/FasL interaction in angiogenesis.
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Abbreviations
- Fas:
-
Factor associated with suicide
- FasL:
-
Fas ligand
- TNF:
-
Tumor necrosis factor
- FADD:
-
Fas-associated death domain protein
- FLIP:
-
Flice-like inhibitory protein
- NF-κB:
-
Nuclear factor Κb
- VEGF:
-
Vascular endothelial growth factor
- EMSA:
-
Electrophoretic mobility shift assay
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Acknowledgments
This work was supported by Grants from the National Natural Science Foundation of China (81171659) and the Natural Science Foundation of Jiangsu Province (BE2010768) to C.B. Zhang.
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Zhang, C., Gao, F., Teng, F. et al. Fas/FasL Complex Promotes Proliferation and Migration of Brain Endothelial Cells Via FADD–FLIP–TRAF–NF-κB Pathway. Cell Biochem Biophys 71, 1319–1323 (2015). https://doi.org/10.1007/s12013-014-0351-4
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DOI: https://doi.org/10.1007/s12013-014-0351-4