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IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis
IL-17B is a member of the IL-17 cytokine family which have been implicated in inflammatory response and autoimmune diseases such as rheumatoid arthritis. The founding member of this family, IL-17 (or IL-17A), has also been implicated in promoting tumour angiogenesis through the induction of other pr...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866247/ https://www.ncbi.nlm.nih.gov/pubmed/20467469 http://dx.doi.org/10.1155/2010/817375 |
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author | Sanders, Andrew J. Guo, Xiaoxia Mason, Malcolm D. Jiang, Wen G. |
author_facet | Sanders, Andrew J. Guo, Xiaoxia Mason, Malcolm D. Jiang, Wen G. |
author_sort | Sanders, Andrew J. |
collection | PubMed |
description | IL-17B is a member of the IL-17 cytokine family which have been implicated in inflammatory response and autoimmune diseases such as rheumatoid arthritis. The founding member of this family, IL-17 (or IL-17A), has also been implicated in promoting tumour angiogenesis through the induction of other proangiogenic factors. Here we examine the potential of recombinant human IL-17B to contribute to the angiogenic process. In vitro rhIL-17B was able to inhibit HECV endothelial cell-matrix adhesion and cellular migration and also, at higher concentrations, could substantially reduce tubule formation compared to untreated HECV cells in a Matrigel tubule formation assay. This data suggests that IL-17B may act in an antiangiogenic manner. |
format | Text |
id | pubmed-2866247 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-28662472010-05-13 IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis Sanders, Andrew J. Guo, Xiaoxia Mason, Malcolm D. Jiang, Wen G. J Oncol Research Article IL-17B is a member of the IL-17 cytokine family which have been implicated in inflammatory response and autoimmune diseases such as rheumatoid arthritis. The founding member of this family, IL-17 (or IL-17A), has also been implicated in promoting tumour angiogenesis through the induction of other proangiogenic factors. Here we examine the potential of recombinant human IL-17B to contribute to the angiogenic process. In vitro rhIL-17B was able to inhibit HECV endothelial cell-matrix adhesion and cellular migration and also, at higher concentrations, could substantially reduce tubule formation compared to untreated HECV cells in a Matrigel tubule formation assay. This data suggests that IL-17B may act in an antiangiogenic manner. Hindawi Publishing Corporation 2010 2010-05-06 /pmc/articles/PMC2866247/ /pubmed/20467469 http://dx.doi.org/10.1155/2010/817375 Text en Copyright © 2010 Andrew J. Sanders et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Sanders, Andrew J. Guo, Xiaoxia Mason, Malcolm D. Jiang, Wen G. IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis |
title | IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis |
title_full | IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis |
title_fullStr | IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis |
title_full_unstemmed | IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis |
title_short | IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis |
title_sort | il-17b can impact on endothelial cellular traits linked to tumour angiogenesis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866247/ https://www.ncbi.nlm.nih.gov/pubmed/20467469 http://dx.doi.org/10.1155/2010/817375 |
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