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 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
facet_avail Online
Free
finc_class_facet Medizin
format ElectronicArticle
fullrecord blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAzOC9qY2JmbS4yMDEwLjEzOA
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAzOC9qY2JmbS4yMDEwLjEzOA
institution DE-Zwi2
DE-D161
DE-Gla1
DE-Zi4
DE-15
DE-Pl11
DE-Rs1
DE-105
DE-14
DE-Ch1
DE-L229
DE-D275
DE-Bn3
DE-Brt1
imprint SAGE Publications, 2011
imprint_str_mv SAGE Publications, 2011
issn 0271-678X
1559-7016
issn_str_mv 0271-678X
1559-7016
language English
mega_collection SAGE Publications (CrossRef)
match_str wang2011tumornecrosisfactoraprimescerebralendothelialcellsforerythropoietininducedangiogenesis
publishDateSort 2011
publisher SAGE Publications
recordtype ai
record_format ai
series Journal of Cerebral Blood Flow & Metabolism
source_id 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>
container_issue 2
container_start_page 640
container_title Journal of Cerebral Blood Flow & Metabolism
container_volume 31
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
_version_ 1792335362373189641
geogr_code not assigned
last_indexed 2024-03-01T14:43:21.161Z
geogr_code_person not assigned
openURL url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=Tumor+Necrosis+Factor+%CE%B1+Primes+Cerebral+Endothelial+Cells+for+Erythropoietin-Induced+Angiogenesis&rft.date=2011-02-01&genre=article&issn=1559-7016&volume=31&issue=2&spage=640&epage=647&pages=640-647&jtitle=Journal+of+Cerebral+Blood+Flow+%26+Metabolism&atitle=Tumor+Necrosis+Factor+%CE%B1+Primes+Cerebral+Endothelial+Cells+for+Erythropoietin-Induced+Angiogenesis&aulast=Zhang&aufirst=Zheng+Gang&rft_id=info%3Adoi%2F10.1038%2Fjcbfm.2010.138&rft.language%5B0%5D=eng
SOLR
_version_ 1792335362373189641
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>
doi_str_mv 10.1038/jcbfm.2010.138
facet_avail Online, Free
finc_class_facet Medizin
format ElectronicArticle
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
geogr_code not assigned
geogr_code_person not assigned
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAzOC9qY2JmbS4yMDEwLjEzOA
imprint SAGE Publications, 2011
imprint_str_mv SAGE Publications, 2011
institution DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1
issn 0271-678X, 1559-7016
issn_str_mv 0271-678X, 1559-7016
language English
last_indexed 2024-03-01T14:43:21.161Z
match_str wang2011tumornecrosisfactoraprimescerebralendothelialcellsforerythropoietininducedangiogenesis
mega_collection SAGE Publications (CrossRef)
physical 640-647
publishDate 2011
publishDateSort 2011
publisher SAGE Publications
record_format ai
recordtype ai
series Journal of Cerebral Blood Flow & Metabolism
source_id 49
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