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Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis
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Zeitschriftentitel: | Journal of Cerebral Blood Flow & Metabolism |
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Personen und Körperschaften: | , , , , , , , , , , , |
In: | Journal of Cerebral Blood Flow & Metabolism, 31, 2011, 2, S. 640-647 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
SAGE Publications
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Schlagwörter: |
author_facet |
Wang, Lei Chopp, Michael Teng, Hua Bolz, Marianne Francisco, Moniche Ãlvarez Aluigi, Danielle Marie Wang, Xin Li Zhang, Rui Lan Chrsitensen, Søren Sager, Thomas N Szalad, Alexandra Zhang, Zheng Gang Wang, Lei Chopp, Michael Teng, Hua Bolz, Marianne Francisco, Moniche Ãlvarez Aluigi, Danielle Marie Wang, Xin Li Zhang, Rui Lan Chrsitensen, Søren Sager, Thomas N Szalad, Alexandra Zhang, Zheng Gang |
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author |
Wang, Lei Chopp, Michael Teng, Hua Bolz, Marianne Francisco, Moniche Ãlvarez Aluigi, Danielle Marie Wang, Xin Li Zhang, Rui Lan Chrsitensen, Søren Sager, Thomas N Szalad, Alexandra Zhang, Zheng Gang |
spellingShingle |
Wang, Lei Chopp, Michael Teng, Hua Bolz, Marianne Francisco, Moniche Ãlvarez Aluigi, Danielle Marie Wang, Xin Li Zhang, Rui Lan Chrsitensen, Søren Sager, Thomas N Szalad, Alexandra Zhang, Zheng Gang Journal of Cerebral Blood Flow & Metabolism Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis Cardiology and Cardiovascular Medicine Neurology (clinical) Neurology |
author_sort |
wang, lei |
spelling |
Wang, Lei Chopp, Michael Teng, Hua Bolz, Marianne Francisco, Moniche Ãlvarez Aluigi, Danielle Marie Wang, Xin Li Zhang, Rui Lan Chrsitensen, Søren Sager, Thomas N Szalad, Alexandra Zhang, Zheng Gang 0271-678X 1559-7016 SAGE Publications Cardiology and Cardiovascular Medicine Neurology (clinical) Neurology http://dx.doi.org/10.1038/jcbfm.2010.138 <jats:p>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.</jats:p> Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis Journal of Cerebral Blood Flow & Metabolism |
doi_str_mv |
10.1038/jcbfm.2010.138 |
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Online Free |
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Medizin |
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SAGE Publications, 2011 |
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SAGE Publications, 2011 |
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2011 |
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SAGE Publications |
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Journal of Cerebral Blood Flow & Metabolism |
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49 |
title |
Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_unstemmed |
Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_full |
Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_fullStr |
Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_full_unstemmed |
Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_short |
Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_sort |
tumor necrosis factor α primes cerebral endothelial cells for erythropoietin-induced angiogenesis |
topic |
Cardiology and Cardiovascular Medicine Neurology (clinical) Neurology |
url |
http://dx.doi.org/10.1038/jcbfm.2010.138 |
publishDate |
2011 |
physical |
640-647 |
description |
<jats:p>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.</jats:p> |
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author | Wang, Lei, Chopp, Michael, Teng, Hua, Bolz, Marianne, Francisco, Moniche Ãlvarez, Aluigi, Danielle Marie, Wang, Xin Li, Zhang, Rui Lan, Chrsitensen, Søren, Sager, Thomas N, Szalad, Alexandra, Zhang, Zheng Gang |
author_facet | Wang, Lei, Chopp, Michael, Teng, Hua, Bolz, Marianne, Francisco, Moniche Ãlvarez, Aluigi, Danielle Marie, Wang, Xin Li, Zhang, Rui Lan, Chrsitensen, Søren, Sager, Thomas N, Szalad, Alexandra, Zhang, Zheng Gang, Wang, Lei, Chopp, Michael, Teng, Hua, Bolz, Marianne, Francisco, Moniche Ãlvarez, Aluigi, Danielle Marie, Wang, Xin Li, Zhang, Rui Lan, Chrsitensen, Søren, Sager, Thomas N, Szalad, Alexandra, Zhang, Zheng Gang |
author_sort | wang, lei |
container_issue | 2 |
container_start_page | 640 |
container_title | Journal of Cerebral Blood Flow & Metabolism |
container_volume | 31 |
description | <jats:p>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.</jats:p> |
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spelling | Wang, Lei Chopp, Michael Teng, Hua Bolz, Marianne Francisco, Moniche Ãlvarez Aluigi, Danielle Marie Wang, Xin Li Zhang, Rui Lan Chrsitensen, Søren Sager, Thomas N Szalad, Alexandra Zhang, Zheng Gang 0271-678X 1559-7016 SAGE Publications Cardiology and Cardiovascular Medicine Neurology (clinical) Neurology http://dx.doi.org/10.1038/jcbfm.2010.138 <jats:p>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.</jats:p> Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis Journal of Cerebral Blood Flow & Metabolism |
spellingShingle | Wang, Lei, Chopp, Michael, Teng, Hua, Bolz, Marianne, Francisco, Moniche Ãlvarez, Aluigi, Danielle Marie, Wang, Xin Li, Zhang, Rui Lan, Chrsitensen, Søren, Sager, Thomas N, Szalad, Alexandra, Zhang, Zheng Gang, Journal of Cerebral Blood Flow & Metabolism, Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis, Cardiology and Cardiovascular Medicine, Neurology (clinical), Neurology |
title | Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_full | Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_fullStr | Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_full_unstemmed | Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_short | Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
title_sort | tumor necrosis factor α primes cerebral endothelial cells for erythropoietin-induced angiogenesis |
title_unstemmed | Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis |
topic | Cardiology and Cardiovascular Medicine, Neurology (clinical), Neurology |
url | http://dx.doi.org/10.1038/jcbfm.2010.138 |