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Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo
Human interferon-inducible protein 10 (IP-10), a member of the alpha chemokine family, inhibits bone marrow colony formation, has antitumor activity in vivo, is chemoattractant for human monocytes and T cells, and promotes T cell adhesion to endothelial cells. Here we report that IP-10 is a potent i...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1995
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192108/ https://www.ncbi.nlm.nih.gov/pubmed/7540647 |
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collection | PubMed |
description | Human interferon-inducible protein 10 (IP-10), a member of the alpha chemokine family, inhibits bone marrow colony formation, has antitumor activity in vivo, is chemoattractant for human monocytes and T cells, and promotes T cell adhesion to endothelial cells. Here we report that IP-10 is a potent inhibitor of angiogenesis in vivo. IP-10 profoundly inhibited basic fibroblast growth factor-induced neovascularization of Matrigel (prepared by H. K. Kleinman) injected subcutaneously into athymic mice. In addition, IP-10, in a dose-dependent fashion, suppressed endothelial cell differentiation into tubular capillary structures in vitro. IP-10 had no effect on endothelial cell growth, attachment, and migration as assayed in vitro. These results document an important biological property of IP-10 and raise the possibility that IP-10 may participate in the regulation of angiogenesis during inflammation and tumorigenesis. |
format | Text |
id | pubmed-2192108 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1995 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21921082008-04-16 Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo J Exp Med Articles Human interferon-inducible protein 10 (IP-10), a member of the alpha chemokine family, inhibits bone marrow colony formation, has antitumor activity in vivo, is chemoattractant for human monocytes and T cells, and promotes T cell adhesion to endothelial cells. Here we report that IP-10 is a potent inhibitor of angiogenesis in vivo. IP-10 profoundly inhibited basic fibroblast growth factor-induced neovascularization of Matrigel (prepared by H. K. Kleinman) injected subcutaneously into athymic mice. In addition, IP-10, in a dose-dependent fashion, suppressed endothelial cell differentiation into tubular capillary structures in vitro. IP-10 had no effect on endothelial cell growth, attachment, and migration as assayed in vitro. These results document an important biological property of IP-10 and raise the possibility that IP-10 may participate in the regulation of angiogenesis during inflammation and tumorigenesis. The Rockefeller University Press 1995-07-01 /pmc/articles/PMC2192108/ /pubmed/7540647 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo |
title | Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo |
title_full | Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo |
title_fullStr | Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo |
title_full_unstemmed | Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo |
title_short | Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo |
title_sort | human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192108/ https://www.ncbi.nlm.nih.gov/pubmed/7540647 |