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Stromal Derived Factor (SDF)‐1 alpha expression in glioma cells & human brain microvascular endothelial cells
Author(s) -
Arteaga Christophe,
Schnee Tona,
Lukyanov Yevgeniy,
Newcomb Elizabeth,
Zagzag David
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a714-c
Subject(s) - downregulation and upregulation , stromal cell , stromal cell derived factor 1 , vascular endothelial growth factor , glioma , tumor necrosis factor alpha , cancer research , biology , cxcr4 , chemistry , chemokine , immunology , vegf receptors , inflammation , biochemistry , gene
The ligand, Stromal Derived Factor (SDF)‐1à and its receptor CXCR4 belong to the Human Chemokine Superfamily. Previous studies have shown that SDF‐1à and CXCR4 knockout mice die perinatally and show hematopoietic, cardiac, and cerebral defects. Hypoxia and Vascular Endothelial Growth Factor (VEGF) have been shown to upregulate CXCR4 in glioma cells. In addition, SDF‐1à has been shown to upregulate Tumor Necrosis Factor (TNF)à. Thus, hypoxia, VEGF and (TNF)à are novel candidates to upregulate SDF‐1à. Immunohistochemistry at the cellular level, Fluorescence Activated Cell Sorting (FACS) analysis, and Western blot were used to determine the level of expression of SDF‐1à. We show that hypoxia upregulates SDF‐1à protein expression in glioma cells after 24 hours. We also propose for the first time that treatment with VEGF and TNFà after 24 hours upregulate SDF‐1à protein expression in Human Brain Microvascular Endothelial Cells. In conclusion, hypoxia, TNFà, and VEGF upregulate SDF‐1à protein expression. Supported by NYU SURP Program, New York University and NIH NIGMS MBRS RISE Grant 5R25 GM059244‐05, Barry University