Stimulation of angiostatic platelet factor-4 variant (CXCL4L1/PF-4var) versus inhibition of angiogenic granulocyte chemotactic protein-2 (CXCL6/GCP-2) in normal and tumoral mesenchymal cells
Chemokines affect inflammation and cancer through leukocyte attraction and angiogenesis. Here, we demonstrate that CXCL4L1/platelet factor‐4 variant (PF‐4var), a highly angiostatic chemokine, is poorly chemotactic for phagocytes and is inducible in monocytes by inflammatory mediators but remained un...
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| Veröffentlicht in: | Journal of leukocyte biology 2007-12, Vol.82 (6), p.1519-1530 |
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| creator | Vandercappellen, Jo Noppen, Samuel Verbeke, Hannelien Put, Willy Conings, René Gouwy, Mieke Schutyser, Evemie Proost, Paul Sciot, Raf Geboes, Karel Opdenakker, Ghislain Van Damme, Jo Struyf, Sofie |
| description | Chemokines affect inflammation and cancer through leukocyte attraction and angiogenesis. Here, we demonstrate that CXCL4L1/platelet factor‐4 variant (PF‐4var), a highly angiostatic chemokine, is poorly chemotactic for phagocytes and is inducible in monocytes by inflammatory mediators but remained undetectable in macrophages and neutrophils. In addition, CXCL4L1/PF‐4var production by mesenchymal tumor cells was evidenced in vitro and in vivo by specific ELISA and immunohistochemistry. CXCL4L1/PF‐4var, but not CXCL4/PF‐4, was coinduced with the angiogenic chemokine CXCL6/granulocyte chemotactic protein‐2 (GCP‐2) by cytokines, e.g., IL‐1β and IL‐17, in sarcoma cells, but not in diploid fibroblasts. Furthermore, the induction of CXCL6/GCP‐2 in endothelial cells by IL‐1β was enhanced synergistically by TNF‐α but inhibited by IFN‐γ, which synergized with IL‐1β to produce the angiostatic CXCL10/IFN‐γ‐induced protein‐10. These findings indicate that the equilibrium between angiostatic and angiogenic factors during inflammation and tumor progression is rather complex and differs depending on the chemokine, cell type, and stimulus. Selective intervention in the chemokine network may drastically disturb this delicate balance of angiogenesis and tissue repair. Application of angiostatic CXCL4L1/PF‐4var without attraction of protumoral phagocytes may be beneficial in cancer therapy. |
| doi_str_mv | 10.1189/jlb.0407206 |
| format | Article |
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Here, we demonstrate that CXCL4L1/platelet factor‐4 variant (PF‐4var), a highly angiostatic chemokine, is poorly chemotactic for phagocytes and is inducible in monocytes by inflammatory mediators but remained undetectable in macrophages and neutrophils. In addition, CXCL4L1/PF‐4var production by mesenchymal tumor cells was evidenced in vitro and in vivo by specific ELISA and immunohistochemistry. CXCL4L1/PF‐4var, but not CXCL4/PF‐4, was coinduced with the angiogenic chemokine CXCL6/granulocyte chemotactic protein‐2 (GCP‐2) by cytokines, e.g., IL‐1β and IL‐17, in sarcoma cells, but not in diploid fibroblasts. Furthermore, the induction of CXCL6/GCP‐2 in endothelial cells by IL‐1β was enhanced synergistically by TNF‐α but inhibited by IFN‐γ, which synergized with IL‐1β to produce the angiostatic CXCL10/IFN‐γ‐induced protein‐10. These findings indicate that the equilibrium between angiostatic and angiogenic factors during inflammation and tumor progression is rather complex and differs depending on the chemokine, cell type, and stimulus. Selective intervention in the chemokine network may drastically disturb this delicate balance of angiogenesis and tissue repair. Application of angiostatic CXCL4L1/PF‐4var without attraction of protumoral phagocytes may be beneficial in cancer therapy.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1189/jlb.0407206</identifier><identifier>PMID: 17827342</identifier><language>eng</language><publisher>United States: Society for Leukocyte Biology</publisher><subject>angiogenesis ; Angiogenesis Inducing Agents - antagonists & inhibitors ; Angiostatic Proteins - immunology ; Antibody Specificity - drug effects ; Cell Adhesion - drug effects ; Cell Line, Tumor ; Cell Movement - drug effects ; chemokine ; Chemokine CXCL6 - antagonists & inhibitors ; Chemotactic Factors - pharmacology ; cytokine ; Cytokines - pharmacology ; Endothelial Cells - cytology ; Endothelial Cells - drug effects ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Humans ; Immunohistochemistry ; Inflammation Mediators ; Kinetics ; Macrophages - cytology ; Macrophages - drug effects ; monocytes ; Monocytes - cytology ; Monocytes - drug effects ; Neovascularization, Physiologic - drug effects ; Neutrophils - cytology ; Neutrophils - drug effects ; Osteosarcoma - pathology ; Phagocytes - cytology ; Phagocytes - drug effects ; Platelet Factor 4 - immunology ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>Journal of leukocyte biology, 2007-12, Vol.82 (6), p.1519-1530</ispartof><rights>2007 Society for Leukocyte Biology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4279-c40a9d84bf02da9201b7bcf1f09954d23f1cea368a68774cb5e55880d188a683</citedby><cites>FETCH-LOGICAL-c4279-c40a9d84bf02da9201b7bcf1f09954d23f1cea368a68774cb5e55880d188a683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1189%2Fjlb.0407206$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1189%2Fjlb.0407206$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17827342$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vandercappellen, Jo</creatorcontrib><creatorcontrib>Noppen, Samuel</creatorcontrib><creatorcontrib>Verbeke, Hannelien</creatorcontrib><creatorcontrib>Put, Willy</creatorcontrib><creatorcontrib>Conings, René</creatorcontrib><creatorcontrib>Gouwy, Mieke</creatorcontrib><creatorcontrib>Schutyser, Evemie</creatorcontrib><creatorcontrib>Proost, Paul</creatorcontrib><creatorcontrib>Sciot, Raf</creatorcontrib><creatorcontrib>Geboes, Karel</creatorcontrib><creatorcontrib>Opdenakker, Ghislain</creatorcontrib><creatorcontrib>Van Damme, Jo</creatorcontrib><creatorcontrib>Struyf, Sofie</creatorcontrib><title>Stimulation of angiostatic platelet factor-4 variant (CXCL4L1/PF-4var) versus inhibition of angiogenic granulocyte chemotactic protein-2 (CXCL6/GCP-2) in normal and tumoral mesenchymal cells</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>Chemokines affect inflammation and cancer through leukocyte attraction and angiogenesis. Here, we demonstrate that CXCL4L1/platelet factor‐4 variant (PF‐4var), a highly angiostatic chemokine, is poorly chemotactic for phagocytes and is inducible in monocytes by inflammatory mediators but remained undetectable in macrophages and neutrophils. In addition, CXCL4L1/PF‐4var production by mesenchymal tumor cells was evidenced in vitro and in vivo by specific ELISA and immunohistochemistry. CXCL4L1/PF‐4var, but not CXCL4/PF‐4, was coinduced with the angiogenic chemokine CXCL6/granulocyte chemotactic protein‐2 (GCP‐2) by cytokines, e.g., IL‐1β and IL‐17, in sarcoma cells, but not in diploid fibroblasts. Furthermore, the induction of CXCL6/GCP‐2 in endothelial cells by IL‐1β was enhanced synergistically by TNF‐α but inhibited by IFN‐γ, which synergized with IL‐1β to produce the angiostatic CXCL10/IFN‐γ‐induced protein‐10. These findings indicate that the equilibrium between angiostatic and angiogenic factors during inflammation and tumor progression is rather complex and differs depending on the chemokine, cell type, and stimulus. Selective intervention in the chemokine network may drastically disturb this delicate balance of angiogenesis and tissue repair. Application of angiostatic CXCL4L1/PF‐4var without attraction of protumoral phagocytes may be beneficial in cancer therapy.</description><subject>angiogenesis</subject><subject>Angiogenesis Inducing Agents - antagonists & inhibitors</subject><subject>Angiostatic Proteins - immunology</subject><subject>Antibody Specificity - drug effects</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>chemokine</subject><subject>Chemokine CXCL6 - antagonists & inhibitors</subject><subject>Chemotactic Factors - pharmacology</subject><subject>cytokine</subject><subject>Cytokines - pharmacology</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - drug effects</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammation Mediators</subject><subject>Kinetics</subject><subject>Macrophages - cytology</subject><subject>Macrophages - drug effects</subject><subject>monocytes</subject><subject>Monocytes - cytology</subject><subject>Monocytes - drug effects</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Neutrophils - cytology</subject><subject>Neutrophils - drug effects</subject><subject>Osteosarcoma - pathology</subject><subject>Phagocytes - cytology</subject><subject>Phagocytes - drug effects</subject><subject>Platelet Factor 4 - immunology</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk-P1CAYh4nRuOPqybvhZNyY7gClhR61cVfNJG7iHrwRSumUDYUV6Dbz5fxsUmei8aIX_vzy5Hnf8ALAS4wuMebN9s52l4giRlD9CGxwU_KirFn5GGwQo7ioKEJn4FmMdwihktToKTjDjBNWUrIBP74mM81WJuMd9AOUbm98TPmu4H2OtdUJDlIlHwoKH2Qw0iX4pv3W7ugOb2-uCprDC_igQ5wjNG40nflLttcuu_ZButl6dUgaqlFPPmXnWiP4pI0ryNFZb6_bm4JcZBF0PkzSZkkP0zz5kM-Tjtqp8bDmSlsbn4Mng7RRvzjt5-D26sNt-7HYfbn-1L7bFYoS1uQVyabntBsQ6WVDEO5YpwY8oKapaE_KASsty5rLmjNGVVfpquIc9ZivUXkOXh-1ud3vs45JTCauDUin_RxFzStKUEP-CxJUMV6xOoNvj6AKPsagB3EfzCTDQWAk1rGKPFZxGmumX520czfp_g97mmMG0BFYjNWHf7nE5917XOVf8rvV0ezHxQQtYn5WmysQsSwLJ6IWv8CfIWa7EQ</recordid><startdate>20071201</startdate><enddate>20071201</enddate><creator>Vandercappellen, Jo</creator><creator>Noppen, Samuel</creator><creator>Verbeke, Hannelien</creator><creator>Put, Willy</creator><creator>Conings, René</creator><creator>Gouwy, Mieke</creator><creator>Schutyser, Evemie</creator><creator>Proost, Paul</creator><creator>Sciot, Raf</creator><creator>Geboes, Karel</creator><creator>Opdenakker, Ghislain</creator><creator>Van Damme, Jo</creator><creator>Struyf, Sofie</creator><general>Society for Leukocyte Biology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20071201</creationdate><title>Stimulation of angiostatic platelet factor-4 variant (CXCL4L1/PF-4var) versus inhibition of angiogenic granulocyte chemotactic protein-2 (CXCL6/GCP-2) in normal and tumoral mesenchymal cells</title><author>Vandercappellen, Jo ; Noppen, Samuel ; Verbeke, Hannelien ; Put, Willy ; Conings, René ; Gouwy, Mieke ; Schutyser, Evemie ; Proost, Paul ; Sciot, Raf ; Geboes, Karel ; Opdenakker, Ghislain ; Van Damme, Jo ; Struyf, Sofie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4279-c40a9d84bf02da9201b7bcf1f09954d23f1cea368a68774cb5e55880d188a683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>angiogenesis</topic><topic>Angiogenesis Inducing Agents - antagonists & inhibitors</topic><topic>Angiostatic Proteins - immunology</topic><topic>Antibody Specificity - drug effects</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>chemokine</topic><topic>Chemokine CXCL6 - antagonists & inhibitors</topic><topic>Chemotactic Factors - pharmacology</topic><topic>cytokine</topic><topic>Cytokines - pharmacology</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - drug effects</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammation Mediators</topic><topic>Kinetics</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>monocytes</topic><topic>Monocytes - cytology</topic><topic>Monocytes - drug effects</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Neutrophils - cytology</topic><topic>Neutrophils - drug effects</topic><topic>Osteosarcoma - pathology</topic><topic>Phagocytes - cytology</topic><topic>Phagocytes - drug effects</topic><topic>Platelet Factor 4 - immunology</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vandercappellen, Jo</creatorcontrib><creatorcontrib>Noppen, Samuel</creatorcontrib><creatorcontrib>Verbeke, Hannelien</creatorcontrib><creatorcontrib>Put, Willy</creatorcontrib><creatorcontrib>Conings, René</creatorcontrib><creatorcontrib>Gouwy, Mieke</creatorcontrib><creatorcontrib>Schutyser, Evemie</creatorcontrib><creatorcontrib>Proost, Paul</creatorcontrib><creatorcontrib>Sciot, Raf</creatorcontrib><creatorcontrib>Geboes, Karel</creatorcontrib><creatorcontrib>Opdenakker, Ghislain</creatorcontrib><creatorcontrib>Van Damme, Jo</creatorcontrib><creatorcontrib>Struyf, Sofie</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vandercappellen, Jo</au><au>Noppen, Samuel</au><au>Verbeke, Hannelien</au><au>Put, Willy</au><au>Conings, René</au><au>Gouwy, Mieke</au><au>Schutyser, Evemie</au><au>Proost, Paul</au><au>Sciot, Raf</au><au>Geboes, Karel</au><au>Opdenakker, Ghislain</au><au>Van Damme, Jo</au><au>Struyf, Sofie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stimulation of angiostatic platelet factor-4 variant (CXCL4L1/PF-4var) versus inhibition of angiogenic granulocyte chemotactic protein-2 (CXCL6/GCP-2) in normal and tumoral mesenchymal cells</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>2007-12-01</date><risdate>2007</risdate><volume>82</volume><issue>6</issue><spage>1519</spage><epage>1530</epage><pages>1519-1530</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>Chemokines affect inflammation and cancer through leukocyte attraction and angiogenesis. Here, we demonstrate that CXCL4L1/platelet factor‐4 variant (PF‐4var), a highly angiostatic chemokine, is poorly chemotactic for phagocytes and is inducible in monocytes by inflammatory mediators but remained undetectable in macrophages and neutrophils. In addition, CXCL4L1/PF‐4var production by mesenchymal tumor cells was evidenced in vitro and in vivo by specific ELISA and immunohistochemistry. CXCL4L1/PF‐4var, but not CXCL4/PF‐4, was coinduced with the angiogenic chemokine CXCL6/granulocyte chemotactic protein‐2 (GCP‐2) by cytokines, e.g., IL‐1β and IL‐17, in sarcoma cells, but not in diploid fibroblasts. Furthermore, the induction of CXCL6/GCP‐2 in endothelial cells by IL‐1β was enhanced synergistically by TNF‐α but inhibited by IFN‐γ, which synergized with IL‐1β to produce the angiostatic CXCL10/IFN‐γ‐induced protein‐10. These findings indicate that the equilibrium between angiostatic and angiogenic factors during inflammation and tumor progression is rather complex and differs depending on the chemokine, cell type, and stimulus. Selective intervention in the chemokine network may drastically disturb this delicate balance of angiogenesis and tissue repair. Application of angiostatic CXCL4L1/PF‐4var without attraction of protumoral phagocytes may be beneficial in cancer therapy.</abstract><cop>United States</cop><pub>Society for Leukocyte Biology</pub><pmid>17827342</pmid><doi>10.1189/jlb.0407206</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Wiley Online Library Journals Frontfile Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | angiogenesis Angiogenesis Inducing Agents - antagonists & inhibitors Angiostatic Proteins - immunology Antibody Specificity - drug effects Cell Adhesion - drug effects Cell Line, Tumor Cell Movement - drug effects chemokine Chemokine CXCL6 - antagonists & inhibitors Chemotactic Factors - pharmacology cytokine Cytokines - pharmacology Endothelial Cells - cytology Endothelial Cells - drug effects Fibroblasts - cytology Fibroblasts - drug effects Humans Immunohistochemistry Inflammation Mediators Kinetics Macrophages - cytology Macrophages - drug effects monocytes Monocytes - cytology Monocytes - drug effects Neovascularization, Physiologic - drug effects Neutrophils - cytology Neutrophils - drug effects Osteosarcoma - pathology Phagocytes - cytology Phagocytes - drug effects Platelet Factor 4 - immunology Tumor Necrosis Factor-alpha - pharmacology |
| title | Stimulation of angiostatic platelet factor-4 variant (CXCL4L1/PF-4var) versus inhibition of angiogenic granulocyte chemotactic protein-2 (CXCL6/GCP-2) in normal and tumoral mesenchymal cells |
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