The anti-angiogenic activity of IL-12 is increased in iNOS−/− mice and involves NK cells
We have previously reported that the in vivo transfer of murine interleukin-12 (IL-12) gene using a Semliki Forest virus vector induced tumor regression through inhibition of tumor blood vessel formation. To examine whether IL-12 anti-angiogenic activity interferes with the NO pathway, we used induc...
Gespeichert in:
Veröffentlicht in: | Journal of molecular medicine (Berlin, Germany) Germany), 2010-08, Vol.88 (8), p.775-784 |
---|---|
Hauptverfasser: | , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 784 |
---|---|
container_issue | 8 |
container_start_page | 775 |
container_title | Journal of molecular medicine (Berlin, Germany) |
container_volume | 88 |
creator | Bielawska-Pohl, Aleksandra Blesson, Séverine Benlalam, Houssem Trenado, Aurélie Opolon, Paule Bawa, Olivia Rouffiac, Valérie Dus, Danuta Kieda, Claudine Chouaib, Salem |
description | We have previously reported that the in vivo transfer of murine interleukin-12 (IL-12) gene using a Semliki Forest virus vector induced tumor regression through inhibition of tumor blood vessel formation. To examine whether IL-12 anti-angiogenic activity interferes with the NO pathway, we used inducible nitric oxide synthase-deficient mice (iNOS
−
/
−
) and demonstrated that the anti-tumor effect of IL-12 is more pronounced in these mice. In addition, despite the increased level of intratumoral VEGF in iNOS
−
/
−
mice, IL-12 induced a stronger inhibition of blood vessel formation. Histological analysis of SFV-IL-12-treated tumors showed an increase in natural killer (NK) perivascular infiltration in iNOS
−
/
−
as compared to control mice. In vitro IL-12-stimulated murine splenic NK cells displayed significant killing activity towards established murine endothelial cells used as targets. These studies indicate that the anti-angiogenic activity of IL-12 interferes with iNOS pathway and involves NK cell recruitment. |
doi_str_mv | 10.1007/s00109-010-0620-7 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_746310300</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2080637101</sourcerecordid><originalsourceid>FETCH-LOGICAL-c432t-7177d278b2169c2336d25e1ca3a3635bab294fdabd81b9bb08a38e5aa506cf2d3</originalsourceid><addsrcrecordid>eNqFkd9KHDEUxoNUdLvtA_SmhELpVfTk_-RSRKu46EXtXSFkMpltZHZGk9kF36DXPmKfxAy7VSiUXuQkJL_zfSd8CH2gcEQB9HEGoGBIKQQUA6L30IwKzggVAt6gGRihCNNUHaK3Od8VWksjDtAhA15xZfgM_bj9GbDrx0hcv4zDMvTRY-fHuInjIx5afLkglOGYcex9Ci6HppxwvL759vvX03FZeBX9JDHdb4ZuEzK-vsI-dF1-h_Zb1-XwfrfP0ffzs9vTC7K4-Xp5erIgvgw7Ek21bpiuakaV8Yxz1TAZqHfcccVl7WpmRNu4uqlobeoaKserIJ2ToHzLGj5HX7a692l4WIc82lXM0wSuD8M6Wy0Up8AB_k8WcylENZGf_iLvhnXqyzesAmMkVXKC6Bbyacg5hdbep7hy6dFSsFNEdhuRLcVOERWDOfq4E17Xq9C8dPzJpACfd4DL3nVtcr2P-ZXjIDSVsnBsy-Xy1C9Dep3w3-7P90qnZA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>609951650</pqid></control><display><type>article</type><title>The anti-angiogenic activity of IL-12 is increased in iNOS−/− mice and involves NK cells</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Bielawska-Pohl, Aleksandra ; Blesson, Séverine ; Benlalam, Houssem ; Trenado, Aurélie ; Opolon, Paule ; Bawa, Olivia ; Rouffiac, Valérie ; Dus, Danuta ; Kieda, Claudine ; Chouaib, Salem</creator><creatorcontrib>Bielawska-Pohl, Aleksandra ; Blesson, Séverine ; Benlalam, Houssem ; Trenado, Aurélie ; Opolon, Paule ; Bawa, Olivia ; Rouffiac, Valérie ; Dus, Danuta ; Kieda, Claudine ; Chouaib, Salem</creatorcontrib><description>We have previously reported that the in vivo transfer of murine interleukin-12 (IL-12) gene using a Semliki Forest virus vector induced tumor regression through inhibition of tumor blood vessel formation. To examine whether IL-12 anti-angiogenic activity interferes with the NO pathway, we used inducible nitric oxide synthase-deficient mice (iNOS
−
/
−
) and demonstrated that the anti-tumor effect of IL-12 is more pronounced in these mice. In addition, despite the increased level of intratumoral VEGF in iNOS
−
/
−
mice, IL-12 induced a stronger inhibition of blood vessel formation. Histological analysis of SFV-IL-12-treated tumors showed an increase in natural killer (NK) perivascular infiltration in iNOS
−
/
−
as compared to control mice. In vitro IL-12-stimulated murine splenic NK cells displayed significant killing activity towards established murine endothelial cells used as targets. These studies indicate that the anti-angiogenic activity of IL-12 interferes with iNOS pathway and involves NK cell recruitment.</description><identifier>ISSN: 0946-2716</identifier><identifier>EISSN: 1432-1440</identifier><identifier>DOI: 10.1007/s00109-010-0620-7</identifier><identifier>PMID: 20383693</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Animals ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Endothelial Cells - pathology ; Gene Knockout Techniques ; General aspects ; Human Genetics ; Interleukin-12 - immunology ; Internal Medicine ; Killer Cells, Natural - immunology ; Killer Cells, Natural - pathology ; Medical sciences ; Melanoma, Experimental - blood supply ; Melanoma, Experimental - immunology ; Melanoma, Experimental - pathology ; Mice ; Mice, Inbred C57BL ; Molecular Medicine ; Neovascularization, Pathologic - immunology ; Neovascularization, Pathologic - pathology ; Nitric Oxide - immunology ; Nitric Oxide Synthase Type II - genetics ; Original Article ; Semliki Forest virus ; Vascular Endothelial Growth Factor A - immunology</subject><ispartof>Journal of molecular medicine (Berlin, Germany), 2010-08, Vol.88 (8), p.775-784</ispartof><rights>Springer-Verlag 2010</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c432t-7177d278b2169c2336d25e1ca3a3635bab294fdabd81b9bb08a38e5aa506cf2d3</citedby><cites>FETCH-LOGICAL-c432t-7177d278b2169c2336d25e1ca3a3635bab294fdabd81b9bb08a38e5aa506cf2d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00109-010-0620-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00109-010-0620-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23047155$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20383693$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bielawska-Pohl, Aleksandra</creatorcontrib><creatorcontrib>Blesson, Séverine</creatorcontrib><creatorcontrib>Benlalam, Houssem</creatorcontrib><creatorcontrib>Trenado, Aurélie</creatorcontrib><creatorcontrib>Opolon, Paule</creatorcontrib><creatorcontrib>Bawa, Olivia</creatorcontrib><creatorcontrib>Rouffiac, Valérie</creatorcontrib><creatorcontrib>Dus, Danuta</creatorcontrib><creatorcontrib>Kieda, Claudine</creatorcontrib><creatorcontrib>Chouaib, Salem</creatorcontrib><title>The anti-angiogenic activity of IL-12 is increased in iNOS−/− mice and involves NK cells</title><title>Journal of molecular medicine (Berlin, Germany)</title><addtitle>J Mol Med</addtitle><addtitle>J Mol Med (Berl)</addtitle><description>We have previously reported that the in vivo transfer of murine interleukin-12 (IL-12) gene using a Semliki Forest virus vector induced tumor regression through inhibition of tumor blood vessel formation. To examine whether IL-12 anti-angiogenic activity interferes with the NO pathway, we used inducible nitric oxide synthase-deficient mice (iNOS
−
/
−
) and demonstrated that the anti-tumor effect of IL-12 is more pronounced in these mice. In addition, despite the increased level of intratumoral VEGF in iNOS
−
/
−
mice, IL-12 induced a stronger inhibition of blood vessel formation. Histological analysis of SFV-IL-12-treated tumors showed an increase in natural killer (NK) perivascular infiltration in iNOS
−
/
−
as compared to control mice. In vitro IL-12-stimulated murine splenic NK cells displayed significant killing activity towards established murine endothelial cells used as targets. These studies indicate that the anti-angiogenic activity of IL-12 interferes with iNOS pathway and involves NK cell recruitment.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Endothelial Cells - pathology</subject><subject>Gene Knockout Techniques</subject><subject>General aspects</subject><subject>Human Genetics</subject><subject>Interleukin-12 - immunology</subject><subject>Internal Medicine</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - pathology</subject><subject>Medical sciences</subject><subject>Melanoma, Experimental - blood supply</subject><subject>Melanoma, Experimental - immunology</subject><subject>Melanoma, Experimental - pathology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular Medicine</subject><subject>Neovascularization, Pathologic - immunology</subject><subject>Neovascularization, Pathologic - pathology</subject><subject>Nitric Oxide - immunology</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Original Article</subject><subject>Semliki Forest virus</subject><subject>Vascular Endothelial Growth Factor A - immunology</subject><issn>0946-2716</issn><issn>1432-1440</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkd9KHDEUxoNUdLvtA_SmhELpVfTk_-RSRKu46EXtXSFkMpltZHZGk9kF36DXPmKfxAy7VSiUXuQkJL_zfSd8CH2gcEQB9HEGoGBIKQQUA6L30IwKzggVAt6gGRihCNNUHaK3Od8VWksjDtAhA15xZfgM_bj9GbDrx0hcv4zDMvTRY-fHuInjIx5afLkglOGYcex9Ci6HppxwvL759vvX03FZeBX9JDHdb4ZuEzK-vsI-dF1-h_Zb1-XwfrfP0ffzs9vTC7K4-Xp5erIgvgw7Ek21bpiuakaV8Yxz1TAZqHfcccVl7WpmRNu4uqlobeoaKserIJ2ToHzLGj5HX7a692l4WIc82lXM0wSuD8M6Wy0Up8AB_k8WcylENZGf_iLvhnXqyzesAmMkVXKC6Bbyacg5hdbep7hy6dFSsFNEdhuRLcVOERWDOfq4E17Xq9C8dPzJpACfd4DL3nVtcr2P-ZXjIDSVsnBsy-Xy1C9Dep3w3-7P90qnZA</recordid><startdate>20100801</startdate><enddate>20100801</enddate><creator>Bielawska-Pohl, Aleksandra</creator><creator>Blesson, Séverine</creator><creator>Benlalam, Houssem</creator><creator>Trenado, Aurélie</creator><creator>Opolon, Paule</creator><creator>Bawa, Olivia</creator><creator>Rouffiac, Valérie</creator><creator>Dus, Danuta</creator><creator>Kieda, Claudine</creator><creator>Chouaib, Salem</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope></search><sort><creationdate>20100801</creationdate><title>The anti-angiogenic activity of IL-12 is increased in iNOS−/− mice and involves NK cells</title><author>Bielawska-Pohl, Aleksandra ; Blesson, Séverine ; Benlalam, Houssem ; Trenado, Aurélie ; Opolon, Paule ; Bawa, Olivia ; Rouffiac, Valérie ; Dus, Danuta ; Kieda, Claudine ; Chouaib, Salem</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c432t-7177d278b2169c2336d25e1ca3a3635bab294fdabd81b9bb08a38e5aa506cf2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Endothelial Cells - pathology</topic><topic>Gene Knockout Techniques</topic><topic>General aspects</topic><topic>Human Genetics</topic><topic>Interleukin-12 - immunology</topic><topic>Internal Medicine</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - pathology</topic><topic>Medical sciences</topic><topic>Melanoma, Experimental - blood supply</topic><topic>Melanoma, Experimental - immunology</topic><topic>Melanoma, Experimental - pathology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular Medicine</topic><topic>Neovascularization, Pathologic - immunology</topic><topic>Neovascularization, Pathologic - pathology</topic><topic>Nitric Oxide - immunology</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Original Article</topic><topic>Semliki Forest virus</topic><topic>Vascular Endothelial Growth Factor A - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bielawska-Pohl, Aleksandra</creatorcontrib><creatorcontrib>Blesson, Séverine</creatorcontrib><creatorcontrib>Benlalam, Houssem</creatorcontrib><creatorcontrib>Trenado, Aurélie</creatorcontrib><creatorcontrib>Opolon, Paule</creatorcontrib><creatorcontrib>Bawa, Olivia</creatorcontrib><creatorcontrib>Rouffiac, Valérie</creatorcontrib><creatorcontrib>Dus, Danuta</creatorcontrib><creatorcontrib>Kieda, Claudine</creatorcontrib><creatorcontrib>Chouaib, Salem</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bielawska-Pohl, Aleksandra</au><au>Blesson, Séverine</au><au>Benlalam, Houssem</au><au>Trenado, Aurélie</au><au>Opolon, Paule</au><au>Bawa, Olivia</au><au>Rouffiac, Valérie</au><au>Dus, Danuta</au><au>Kieda, Claudine</au><au>Chouaib, Salem</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The anti-angiogenic activity of IL-12 is increased in iNOS−/− mice and involves NK cells</atitle><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle><stitle>J Mol Med</stitle><addtitle>J Mol Med (Berl)</addtitle><date>2010-08-01</date><risdate>2010</risdate><volume>88</volume><issue>8</issue><spage>775</spage><epage>784</epage><pages>775-784</pages><issn>0946-2716</issn><eissn>1432-1440</eissn><abstract>We have previously reported that the in vivo transfer of murine interleukin-12 (IL-12) gene using a Semliki Forest virus vector induced tumor regression through inhibition of tumor blood vessel formation. To examine whether IL-12 anti-angiogenic activity interferes with the NO pathway, we used inducible nitric oxide synthase-deficient mice (iNOS
−
/
−
) and demonstrated that the anti-tumor effect of IL-12 is more pronounced in these mice. In addition, despite the increased level of intratumoral VEGF in iNOS
−
/
−
mice, IL-12 induced a stronger inhibition of blood vessel formation. Histological analysis of SFV-IL-12-treated tumors showed an increase in natural killer (NK) perivascular infiltration in iNOS
−
/
−
as compared to control mice. In vitro IL-12-stimulated murine splenic NK cells displayed significant killing activity towards established murine endothelial cells used as targets. These studies indicate that the anti-angiogenic activity of IL-12 interferes with iNOS pathway and involves NK cell recruitment.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>20383693</pmid><doi>10.1007/s00109-010-0620-7</doi><tpages>10</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0946-2716 |
ispartof | Journal of molecular medicine (Berlin, Germany), 2010-08, Vol.88 (8), p.775-784 |
issn | 0946-2716 1432-1440 |
language | eng |
recordid | cdi_proquest_miscellaneous_746310300 |
source | MEDLINE; SpringerLink Journals - AutoHoldings |
subjects | Animals Biological and medical sciences Biomedical and Life Sciences Biomedicine Endothelial Cells - pathology Gene Knockout Techniques General aspects Human Genetics Interleukin-12 - immunology Internal Medicine Killer Cells, Natural - immunology Killer Cells, Natural - pathology Medical sciences Melanoma, Experimental - blood supply Melanoma, Experimental - immunology Melanoma, Experimental - pathology Mice Mice, Inbred C57BL Molecular Medicine Neovascularization, Pathologic - immunology Neovascularization, Pathologic - pathology Nitric Oxide - immunology Nitric Oxide Synthase Type II - genetics Original Article Semliki Forest virus Vascular Endothelial Growth Factor A - immunology |
title | The anti-angiogenic activity of IL-12 is increased in iNOS−/− mice and involves NK cells |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T21%3A30%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20anti-angiogenic%20activity%20of%20IL-12%20is%20increased%20in%20iNOS%E2%88%92/%E2%88%92%20mice%20and%20involves%20NK%20cells&rft.jtitle=Journal%20of%20molecular%20medicine%20(Berlin,%20Germany)&rft.au=Bielawska-Pohl,%20Aleksandra&rft.date=2010-08-01&rft.volume=88&rft.issue=8&rft.spage=775&rft.epage=784&rft.pages=775-784&rft.issn=0946-2716&rft.eissn=1432-1440&rft_id=info:doi/10.1007/s00109-010-0620-7&rft_dat=%3Cproquest_cross%3E2080637101%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=609951650&rft_id=info:pmid/20383693&rfr_iscdi=true |