Interleukin-18/Interleukin-18 Binding Protein Signaling Modulates Ischemia-Induced Neovascularization in Mice Hindlimb
ABSTRACT—Identification of factors that may stimulate ischemia-induced neovascularization without increasing atherosclerotic plaque progression is of major therapeutic importance. We hypothesized that interleukin-18 binding protein (IL-18BP), a major antiinflammatory protein with plaque-stabilizing...
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| Veröffentlicht in: | Circulation research 2002-09, Vol.91 (5), p.441-448 |
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| creator | Mallat, Ziad Silvestre, Jean-Sébastien Le Ricousse-Roussanne, Sophie Lecomte-Raclet, Laurence Corbaz, Anne Clergue, Michel Duriez, Micheline Barateau, Véronique Akira, Shizuo Tedgui, Alain Tobelem, Gérard Chvatchko, Yolande Lévy, Bernard I |
| description | ABSTRACT—Identification of factors that may stimulate ischemia-induced neovascularization without increasing atherosclerotic plaque progression is of major therapeutic importance. We hypothesized that interleukin-18 binding protein (IL-18BP), a major antiinflammatory protein with plaque-stabilizing activities, may affect the neovascularization in mice ischemic hindlimb. Ischemia was produced by artery femoral occlusion in mice that were subjected to in vivo intramuscular electrotransfer of either an empty plasmid or a murine IL-18BP plasmid. Angiographic score, capillary density (CD31 staining), and laser Doppler perfusion data at day 28 showed significant improvement in ischemic/nonischemic leg ratio by respectively 1.6-, 1.4-, and 1.5-fold in IL-18BP–treated mice compared with controls (P |
| doi_str_mv | 10.1161/01.RES.0000033592.11674.D8 |
| format | Article |
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We hypothesized that interleukin-18 binding protein (IL-18BP), a major antiinflammatory protein with plaque-stabilizing activities, may affect the neovascularization in mice ischemic hindlimb. Ischemia was produced by artery femoral occlusion in mice that were subjected to in vivo intramuscular electrotransfer of either an empty plasmid or a murine IL-18BP plasmid. Angiographic score, capillary density (CD31 staining), and laser Doppler perfusion data at day 28 showed significant improvement in ischemic/nonischemic leg ratio by respectively 1.6-, 1.4-, and 1.5-fold in IL-18BP–treated mice compared with controls (P <0.01). This was associated with a significant 2-fold increase in both vascular endothelial growth factor (VEGF) and phospho-Akt protein content in the ischemic hindlimb of IL-18BP–treated mice (P <0.05). Similar results were obtained in IL-18–deficient mice. Because bone marrow–derived endothelial progenitor cells (BM-EPCs) are involved in postnatal vasculogenesis, EPCs were isolated and cultivated from bone marrow mononuclear cells. IL-18BP treatment led to a significant 1.8-fold increase in the percentage of BM-EPCs characterized as cells positive for both AcLDL-Dil and von Willebrand factor (P <0.001). In conclusion, IL-18BP stimulates ischemia-induced neovascularization in association with an activation of VEGF/Akt signaling and an increase in BM-EPCs mobilization and differentiation. Our findings strongly suggest a major antiangiogenic role of endogenous IL-18 in postischemic injury.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.0000033592.11674.D8</identifier><identifier>PMID: 12215494</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Angiography ; Animals ; Biological and medical sciences ; Blood and lymphatic vessels ; Bone Marrow Cells - cytology ; Bone Marrow Cells - drug effects ; Bone Marrow Cells - physiology ; Cardiology. Vascular system ; Cell Line ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Endothelial Growth Factors - metabolism ; Endothelial Growth Factors - pharmacology ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Glycoproteins - genetics ; Glycoproteins - physiology ; Hindlimb - blood supply ; Hindlimb - metabolism ; Humans ; Intercellular Signaling Peptides and Proteins - metabolism ; Intercellular Signaling Peptides and Proteins - pharmacology ; Interleukin-18 - genetics ; Interleukin-18 - pharmacology ; Interleukin-18 - physiology ; Ischemia - physiopathology ; Laser-Doppler Flowmetry ; Lymphokines - metabolism ; Lymphokines - pharmacology ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neovascularization, Pathologic - physiopathology ; Neovascularization, Physiologic - drug effects ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Phosphorylation ; Plasmids - administration & dosage ; Plasmids - genetics ; Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-akt ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors</subject><ispartof>Circulation research, 2002-09, Vol.91 (5), p.441-448</ispartof><rights>2002 American Heart Association, Inc.</rights><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Sep 6, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5712-52ced1e98aa2f253f593ce42476c7a00e6644e8732e2ba79fd6dd4d3f2eb9813</citedby><cites>FETCH-LOGICAL-c5712-52ced1e98aa2f253f593ce42476c7a00e6644e8732e2ba79fd6dd4d3f2eb9813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13913066$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12215494$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mallat, Ziad</creatorcontrib><creatorcontrib>Silvestre, Jean-Sébastien</creatorcontrib><creatorcontrib>Le Ricousse-Roussanne, Sophie</creatorcontrib><creatorcontrib>Lecomte-Raclet, Laurence</creatorcontrib><creatorcontrib>Corbaz, Anne</creatorcontrib><creatorcontrib>Clergue, Michel</creatorcontrib><creatorcontrib>Duriez, Micheline</creatorcontrib><creatorcontrib>Barateau, Véronique</creatorcontrib><creatorcontrib>Akira, Shizuo</creatorcontrib><creatorcontrib>Tedgui, Alain</creatorcontrib><creatorcontrib>Tobelem, Gérard</creatorcontrib><creatorcontrib>Chvatchko, Yolande</creatorcontrib><creatorcontrib>Lévy, Bernard I</creatorcontrib><title>Interleukin-18/Interleukin-18 Binding Protein Signaling Modulates Ischemia-Induced Neovascularization in Mice Hindlimb</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>ABSTRACT—Identification of factors that may stimulate ischemia-induced neovascularization without increasing atherosclerotic plaque progression is of major therapeutic importance. We hypothesized that interleukin-18 binding protein (IL-18BP), a major antiinflammatory protein with plaque-stabilizing activities, may affect the neovascularization in mice ischemic hindlimb. Ischemia was produced by artery femoral occlusion in mice that were subjected to in vivo intramuscular electrotransfer of either an empty plasmid or a murine IL-18BP plasmid. Angiographic score, capillary density (CD31 staining), and laser Doppler perfusion data at day 28 showed significant improvement in ischemic/nonischemic leg ratio by respectively 1.6-, 1.4-, and 1.5-fold in IL-18BP–treated mice compared with controls (P <0.01). This was associated with a significant 2-fold increase in both vascular endothelial growth factor (VEGF) and phospho-Akt protein content in the ischemic hindlimb of IL-18BP–treated mice (P <0.05). Similar results were obtained in IL-18–deficient mice. Because bone marrow–derived endothelial progenitor cells (BM-EPCs) are involved in postnatal vasculogenesis, EPCs were isolated and cultivated from bone marrow mononuclear cells. IL-18BP treatment led to a significant 1.8-fold increase in the percentage of BM-EPCs characterized as cells positive for both AcLDL-Dil and von Willebrand factor (P <0.001). In conclusion, IL-18BP stimulates ischemia-induced neovascularization in association with an activation of VEGF/Akt signaling and an increase in BM-EPCs mobilization and differentiation. Our findings strongly suggest a major antiangiogenic role of endogenous IL-18 in postischemic injury.</description><subject>Angiography</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Bone Marrow Cells - cytology</subject><subject>Bone Marrow Cells - drug effects</subject><subject>Bone Marrow Cells - physiology</subject><subject>Cardiology. Vascular system</subject><subject>Cell Line</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Endothelial Growth Factors - metabolism</subject><subject>Endothelial Growth Factors - pharmacology</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Glycoproteins - genetics</subject><subject>Glycoproteins - physiology</subject><subject>Hindlimb - blood supply</subject><subject>Hindlimb - metabolism</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - pharmacology</subject><subject>Interleukin-18 - genetics</subject><subject>Interleukin-18 - pharmacology</subject><subject>Interleukin-18 - physiology</subject><subject>Ischemia - physiopathology</subject><subject>Laser-Doppler Flowmetry</subject><subject>Lymphokines - metabolism</subject><subject>Lymphokines - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neovascularization, Pathologic - physiopathology</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Phosphorylation</subject><subject>Plasmids - administration & dosage</subject><subject>Plasmids - genetics</subject><subject>Protein-Serine-Threonine Kinases</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Vascular Endothelial Growth Factor A</subject><subject>Vascular Endothelial Growth Factors</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd1u1DAQhS0EokvhFVBUCe6yHf8kjrmDttCVWkC095bXmXTdOk5rJ63g6XG6K63AN5ZnvjnjmUPIEYUlpTU9Brr8dXa1hPlwXik2h6VYnjYvyIJWTJSikvQlWeS8KiXncEDepHQLQAVn6jU5oIzRSiixII-rMGL0ON25UNLm-N9n8cWF1oWb4mccRnShuHI3wfg5cjm0kzcjpmKV7AZ7Z8pVaCeLbfEdh0eTbE5H98eMbghFLr10FovzrOddv35LXnXGJ3y3uw_J9dez65Pz8uLHt9XJ54vS5glYWbGsR1E1xrCOVbyrFLcomJC1lQYA61oIbCRnyNZGqq6t21a0vGO4Vg3lh-TjVvY-Dg8TplH3Lln03gQcpqQlg1pCBRk8-g-8HaaYR02aUSYYAGsy9GkL2TikFLHT99H1Jv7WFPTsjAaqszN674x-dkafzsXvdx2mdY_tvnRnRQY-7IC8O-O7aIJ1ac9xRTnUdebElnsafPYq3fnpCaPeoPHj5rk1h7y6-cugoIYyRyjjfwGSE6a8</recordid><startdate>20020906</startdate><enddate>20020906</enddate><creator>Mallat, Ziad</creator><creator>Silvestre, Jean-Sébastien</creator><creator>Le Ricousse-Roussanne, Sophie</creator><creator>Lecomte-Raclet, Laurence</creator><creator>Corbaz, Anne</creator><creator>Clergue, Michel</creator><creator>Duriez, Micheline</creator><creator>Barateau, Véronique</creator><creator>Akira, Shizuo</creator><creator>Tedgui, Alain</creator><creator>Tobelem, Gérard</creator><creator>Chvatchko, Yolande</creator><creator>Lévy, Bernard I</creator><general>American Heart Association, Inc</general><general>Lippincott</general><general>Lippincott Williams & Wilkins Ovid Technologies</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20020906</creationdate><title>Interleukin-18/Interleukin-18 Binding Protein Signaling Modulates Ischemia-Induced Neovascularization in Mice Hindlimb</title><author>Mallat, Ziad ; Silvestre, Jean-Sébastien ; Le Ricousse-Roussanne, Sophie ; Lecomte-Raclet, Laurence ; Corbaz, Anne ; Clergue, Michel ; Duriez, Micheline ; Barateau, Véronique ; Akira, Shizuo ; Tedgui, Alain ; Tobelem, Gérard ; Chvatchko, Yolande ; Lévy, Bernard I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5712-52ced1e98aa2f253f593ce42476c7a00e6644e8732e2ba79fd6dd4d3f2eb9813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Angiography</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Bone Marrow Cells - cytology</topic><topic>Bone Marrow Cells - drug effects</topic><topic>Bone Marrow Cells - physiology</topic><topic>Cardiology. Vascular system</topic><topic>Cell Line</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Endothelial Growth Factors - metabolism</topic><topic>Endothelial Growth Factors - pharmacology</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Glycoproteins - genetics</topic><topic>Glycoproteins - physiology</topic><topic>Hindlimb - blood supply</topic><topic>Hindlimb - metabolism</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Intercellular Signaling Peptides and Proteins - pharmacology</topic><topic>Interleukin-18 - genetics</topic><topic>Interleukin-18 - pharmacology</topic><topic>Interleukin-18 - physiology</topic><topic>Ischemia - physiopathology</topic><topic>Laser-Doppler Flowmetry</topic><topic>Lymphokines - metabolism</topic><topic>Lymphokines - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Neovascularization, Pathologic - physiopathology</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Phosphorylation</topic><topic>Plasmids - administration & dosage</topic><topic>Plasmids - genetics</topic><topic>Protein-Serine-Threonine Kinases</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Vascular Endothelial Growth Factor A</topic><topic>Vascular Endothelial Growth Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mallat, Ziad</creatorcontrib><creatorcontrib>Silvestre, Jean-Sébastien</creatorcontrib><creatorcontrib>Le Ricousse-Roussanne, Sophie</creatorcontrib><creatorcontrib>Lecomte-Raclet, Laurence</creatorcontrib><creatorcontrib>Corbaz, Anne</creatorcontrib><creatorcontrib>Clergue, Michel</creatorcontrib><creatorcontrib>Duriez, Micheline</creatorcontrib><creatorcontrib>Barateau, Véronique</creatorcontrib><creatorcontrib>Akira, Shizuo</creatorcontrib><creatorcontrib>Tedgui, Alain</creatorcontrib><creatorcontrib>Tobelem, Gérard</creatorcontrib><creatorcontrib>Chvatchko, Yolande</creatorcontrib><creatorcontrib>Lévy, Bernard I</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mallat, Ziad</au><au>Silvestre, Jean-Sébastien</au><au>Le Ricousse-Roussanne, Sophie</au><au>Lecomte-Raclet, Laurence</au><au>Corbaz, Anne</au><au>Clergue, Michel</au><au>Duriez, Micheline</au><au>Barateau, Véronique</au><au>Akira, Shizuo</au><au>Tedgui, Alain</au><au>Tobelem, Gérard</au><au>Chvatchko, Yolande</au><au>Lévy, Bernard I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin-18/Interleukin-18 Binding Protein Signaling Modulates Ischemia-Induced Neovascularization in Mice Hindlimb</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2002-09-06</date><risdate>2002</risdate><volume>91</volume><issue>5</issue><spage>441</spage><epage>448</epage><pages>441-448</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>ABSTRACT—Identification of factors that may stimulate ischemia-induced neovascularization without increasing atherosclerotic plaque progression is of major therapeutic importance. We hypothesized that interleukin-18 binding protein (IL-18BP), a major antiinflammatory protein with plaque-stabilizing activities, may affect the neovascularization in mice ischemic hindlimb. Ischemia was produced by artery femoral occlusion in mice that were subjected to in vivo intramuscular electrotransfer of either an empty plasmid or a murine IL-18BP plasmid. Angiographic score, capillary density (CD31 staining), and laser Doppler perfusion data at day 28 showed significant improvement in ischemic/nonischemic leg ratio by respectively 1.6-, 1.4-, and 1.5-fold in IL-18BP–treated mice compared with controls (P <0.01). This was associated with a significant 2-fold increase in both vascular endothelial growth factor (VEGF) and phospho-Akt protein content in the ischemic hindlimb of IL-18BP–treated mice (P <0.05). Similar results were obtained in IL-18–deficient mice. Because bone marrow–derived endothelial progenitor cells (BM-EPCs) are involved in postnatal vasculogenesis, EPCs were isolated and cultivated from bone marrow mononuclear cells. IL-18BP treatment led to a significant 1.8-fold increase in the percentage of BM-EPCs characterized as cells positive for both AcLDL-Dil and von Willebrand factor (P <0.001). In conclusion, IL-18BP stimulates ischemia-induced neovascularization in association with an activation of VEGF/Akt signaling and an increase in BM-EPCs mobilization and differentiation. Our findings strongly suggest a major antiangiogenic role of endogenous IL-18 in postischemic injury.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>12215494</pmid><doi>10.1161/01.RES.0000033592.11674.D8</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation research, 2002-09, Vol.91 (5), p.441-448 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Angiography Animals Biological and medical sciences Blood and lymphatic vessels Bone Marrow Cells - cytology Bone Marrow Cells - drug effects Bone Marrow Cells - physiology Cardiology. Vascular system Cell Line Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Endothelial Growth Factors - metabolism Endothelial Growth Factors - pharmacology Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Glycoproteins - genetics Glycoproteins - physiology Hindlimb - blood supply Hindlimb - metabolism Humans Intercellular Signaling Peptides and Proteins - metabolism Intercellular Signaling Peptides and Proteins - pharmacology Interleukin-18 - genetics Interleukin-18 - pharmacology Interleukin-18 - physiology Ischemia - physiopathology Laser-Doppler Flowmetry Lymphokines - metabolism Lymphokines - pharmacology Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Neovascularization, Pathologic - physiopathology Neovascularization, Physiologic - drug effects Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Phosphorylation Plasmids - administration & dosage Plasmids - genetics Protein-Serine-Threonine Kinases Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
| title | Interleukin-18/Interleukin-18 Binding Protein Signaling Modulates Ischemia-Induced Neovascularization in Mice Hindlimb |
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