title: Fas/FasL Complex Promotes Proliferation and Migration of Brain Endothelial Cells Via FADD-FLIP-TRAF-NF-κB Pathway.
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.
authors.affiliation: Department of Laboratory Medicine, Jiangsu Province Hosptial of TCM, Nanjing, China.
authors.forename: Chunbing
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Department of Laboratory Medicine, Jiangsu Province Hosptial of TCM, Nanjing, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Gao
authors.affiliation: Department of Laboratory Medicine, Jiangsu Province Hosptial of TCM, Nanjing, China.
authors.forename: Fengmeng
authors.initials: F
authors.lastname: Teng
authors.affiliation: Department of Immunology, Nanjing Medical University, Nanjing, China. mingshunzhang@njmu.edu.cn.
authors.forename: Mingshun
authors.initials: M
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000166:cytology*; D053446:CASP8 and FADD-Like Apoptosis Regulating Protein / Q000378:metabolism; D002465:Cell Movement; D049109:Cell Proliferation; D042783:Endothelial Cells / Q000166:cytology* / Q000378:metabolism; D053222:Fas Ligand Protein / Q000378:metabolism*; D053200:Fas-Associated Death Domain Protein / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics; D015398:Signal Transduction; D012995:Solubility; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / Q000378:metabolism; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D019014:fas Receptor / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*
chemical_list: D053446:CASP8 and FADD-Like Apoptosis Regulating Protein; C506387:Cflar protein, mouse; C505534:Fadd protein, mouse; D053222:Fas Ligand Protein; C491899:Fas protein, mouse; D053200:Fas-Associated Death Domain Protein; D016328:NF-kappa B; D034741:RNA, Small Interfering; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins; D042461:Vascular Endothelial Growth Factor A; D019014:fas Receptor
keywords: Endothelial cell; FasL; NF-κb; Proliferation