scholarly journals Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis

2011 ◽  
Vol 31 (5) ◽  
pp. 1334-1334
Author(s):  
Lei Wang ◽  
Michael Chopp ◽  
Hua Teng ◽  
Marianne Bolz ◽  
Moniche Ãlvarez Francisco ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Cerebral Endothelial Cells ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis

2010 ◽  
Vol 31 (2) ◽  
pp. 640-647 ◽  
Author(s):  
Lei Wang ◽  
Michael Chopp ◽  
Hua Teng ◽  
Marianne Bolz ◽  
Moniche Ãlvarez Francisco ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tube Formation ◽  
Cerebral Endothelial Cells ◽  
Tnf Α ◽  
Factor Α ◽  
Epor Expression ◽  
Necrosis Factor

Erythropoietin (EPO) enhances angiogenesis in the ischemic brain. Stroke induces secretion of tumor necrosis factor α (TNF-α). We investigated the effect of TNF-α on EPO-induced in vitro angiogenesis in cerebral endothelial cells. Using a capillary-like tubular formation assay, we found that transient incubation of primary rat cerebral microvascular endothelial cells (RECs) with TNF-α substantially upregulated EPO receptor (EPOR) expression and addition of EPO into TNF-α-treated RECs significantly augmented the capillary-like tube formation. Blockage of TNF receptor 1 (TNFR1) suppressed TNF-α-upregulated EPOR expression and abolished EPO-induced tube formation. Attenuation of endogenous EPOR with small interfering RNA (siRNA) also inhibited EPO-enhanced tube formation. Treatment of RECs with EPO activated nuclear factor-kappa B (NF-κB) and Akt. Incubation of the TNF-α-treated endothelial cells with EPO activated vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), angiopoietin 1 (Ang1), and Tie2. Blockage of VEGFR2 and Tie2 resulted in reduction of EPO-augmented tube formation. These data indicate that interaction of TNF-α with TNFR1 sensitizes cerebral endothelial cells for EPO-induced angiogenesis by upregulation of EPOR, which amplifies the effect of EPO on activation of the VEGF/VEGFR2 and Ang1/Tie2 pathways. Our results provide the evidence for crosslink between TNF and EPOR to coordinate the onset of angiogenesis in cerebral endothelial cells.

Resveratrol Suppresses Tumor Necrosis Factor-α-Induced Fractalkine Expression in Endothelial Cells

2006 ◽  
Vol 70 (1) ◽  
pp. 112-119 ◽  
Author(s):  
Sang-Ok Moon ◽  
Won Kim ◽  
Mi Jeong Sung ◽  
Sik Lee ◽  
Kyung Pyo Kang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor
Sign in / Sign up

Export Citation Format

Share Document