Decreased angiogenesis and arthritic disease in rabbits treated with an alphavbeta3 antagonist
Rheumatoid arthritis (RA) is an inflammatory disease associated with intense angiogenesis and vascular expression of integrin alphavbeta3. Intra-articular administration of a cyclic peptide antagonist of integrin alphavbeta3 to rabbits with antigen-induced arthritis early in disease resulted in inhi...
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| Veröffentlicht in: | The Journal of clinical investigation 1999-01, Vol.103 (1), p.47-54 |
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| container_title | The Journal of clinical investigation |
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| creator | Storgard, C M Stupack, D G Jonczyk, A Goodman, S L Fox, R I Cheresh, D A |
| description | Rheumatoid arthritis (RA) is an inflammatory disease associated with intense angiogenesis and vascular expression of integrin alphavbeta3. Intra-articular administration of a cyclic peptide antagonist of integrin alphavbeta3 to rabbits with antigen-induced arthritis early in disease resulted in inhibition of synovial angiogenesis and reduced synovial cell infiltrate, pannus formation, and cartilage erosions. These effects were not associated with lymphopenia or impairment of leukocyte function. Furthermore, when administered in chronic, preexisting disease, the alphavbeta3 antagonist effectively diminished arthritis severity and was associated with a quantitative increase in apoptosis of the angiogenic blood vessels. Therefore, angiogenesis appears to be a central factor in the initiation and persistence of arthritic disease, and antagonists of integrin alphavbeta3 may represent a novel therapeutic strategy for RA. |
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Intra-articular administration of a cyclic peptide antagonist of integrin alphavbeta3 to rabbits with antigen-induced arthritis early in disease resulted in inhibition of synovial angiogenesis and reduced synovial cell infiltrate, pannus formation, and cartilage erosions. These effects were not associated with lymphopenia or impairment of leukocyte function. Furthermore, when administered in chronic, preexisting disease, the alphavbeta3 antagonist effectively diminished arthritis severity and was associated with a quantitative increase in apoptosis of the angiogenic blood vessels. Therefore, angiogenesis appears to be a central factor in the initiation and persistence of arthritic disease, and antagonists of integrin alphavbeta3 may represent a novel therapeutic strategy for RA.</description><identifier>ISSN: 0021-9738</identifier><identifier>PMID: 9884333</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Apoptosis - drug effects ; Arthritis - drug therapy ; Arthritis - physiopathology ; Cartilage - drug effects ; Cartilage - pathology ; Cell Movement - drug effects ; Fibroblast Growth Factor 2 - pharmacology ; Fluorescent Antibody Technique ; Immunohistochemistry ; In Situ Nick-End Labeling ; Leukocytes - drug effects ; Neovascularization, Pathologic - drug therapy ; Oligopeptides - physiology ; Oligopeptides - therapeutic use ; Peptides, Cyclic - pharmacology ; Peptides, Cyclic - therapeutic use ; Rabbits ; Receptors, Vitronectin - antagonists & inhibitors ; Receptors, Vitronectin - metabolism ; Synovial Membrane - drug effects ; Synovial Membrane - pathology</subject><ispartof>The Journal of clinical investigation, 1999-01, Vol.103 (1), p.47-54</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9884333$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Storgard, C M</creatorcontrib><creatorcontrib>Stupack, D G</creatorcontrib><creatorcontrib>Jonczyk, A</creatorcontrib><creatorcontrib>Goodman, S L</creatorcontrib><creatorcontrib>Fox, R I</creatorcontrib><creatorcontrib>Cheresh, D A</creatorcontrib><title>Decreased angiogenesis and arthritic disease in rabbits treated with an alphavbeta3 antagonist</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Rheumatoid arthritis (RA) is an inflammatory disease associated with intense angiogenesis and vascular expression of integrin alphavbeta3. Intra-articular administration of a cyclic peptide antagonist of integrin alphavbeta3 to rabbits with antigen-induced arthritis early in disease resulted in inhibition of synovial angiogenesis and reduced synovial cell infiltrate, pannus formation, and cartilage erosions. These effects were not associated with lymphopenia or impairment of leukocyte function. Furthermore, when administered in chronic, preexisting disease, the alphavbeta3 antagonist effectively diminished arthritis severity and was associated with a quantitative increase in apoptosis of the angiogenic blood vessels. Therefore, angiogenesis appears to be a central factor in the initiation and persistence of arthritic disease, and antagonists of integrin alphavbeta3 may represent a novel therapeutic strategy for RA.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Arthritis - drug therapy</subject><subject>Arthritis - physiopathology</subject><subject>Cartilage - drug effects</subject><subject>Cartilage - pathology</subject><subject>Cell Movement - drug effects</subject><subject>Fibroblast Growth Factor 2 - pharmacology</subject><subject>Fluorescent Antibody Technique</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Leukocytes - drug effects</subject><subject>Neovascularization, Pathologic - drug therapy</subject><subject>Oligopeptides - physiology</subject><subject>Oligopeptides - therapeutic use</subject><subject>Peptides, Cyclic - pharmacology</subject><subject>Peptides, Cyclic - therapeutic use</subject><subject>Rabbits</subject><subject>Receptors, Vitronectin - antagonists & inhibitors</subject><subject>Receptors, Vitronectin - metabolism</subject><subject>Synovial Membrane - drug effects</subject><subject>Synovial Membrane - pathology</subject><issn>0021-9738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNotkDtPxDAQhF2AjuPgJyC5ootkx06clOh4SifRXE20jteJUV7YDoh_j9FdNTujb7aYC7JlLOdZrUR1Ra5D-GSMS1nIDdnUVSWFEFvy8YitRwhoKEydmzucMLiQTAp87L2LrqXGhX-Guol60NrFQGNqxdT6cbFPNIVh6eFbYwSRbIRunlyIN-TSwhDw9qw7cnx-Ou5fs8P7y9v-4ZAthRCZsRa1ZFaXXKt0GKi5QllbywumrS05k1YByJwZpixXnCFAbgRwU2BhxY7cn94ufv5aMcRmdKHFYYAJ5zU0ZV3IvFJ5Au_O4KpHNM3i3Qj-tznvIf4AVCtdPg</recordid><startdate>199901</startdate><enddate>199901</enddate><creator>Storgard, C M</creator><creator>Stupack, D G</creator><creator>Jonczyk, A</creator><creator>Goodman, S L</creator><creator>Fox, R I</creator><creator>Cheresh, D A</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>199901</creationdate><title>Decreased angiogenesis and arthritic disease in rabbits treated with an alphavbeta3 antagonist</title><author>Storgard, C M ; Stupack, D G ; Jonczyk, A ; Goodman, S L ; Fox, R I ; Cheresh, D A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p533-dffeb40fb61b7b40da917e49ff150bff6104f7aa420d07f1710eaa2d3a1d5e5f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Arthritis - drug therapy</topic><topic>Arthritis - physiopathology</topic><topic>Cartilage - drug effects</topic><topic>Cartilage - pathology</topic><topic>Cell Movement - drug effects</topic><topic>Fibroblast Growth Factor 2 - pharmacology</topic><topic>Fluorescent Antibody Technique</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>Leukocytes - drug effects</topic><topic>Neovascularization, Pathologic - drug therapy</topic><topic>Oligopeptides - physiology</topic><topic>Oligopeptides - therapeutic use</topic><topic>Peptides, Cyclic - pharmacology</topic><topic>Peptides, Cyclic - therapeutic use</topic><topic>Rabbits</topic><topic>Receptors, Vitronectin - antagonists & inhibitors</topic><topic>Receptors, Vitronectin - metabolism</topic><topic>Synovial Membrane - drug effects</topic><topic>Synovial Membrane - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Storgard, C M</creatorcontrib><creatorcontrib>Stupack, D G</creatorcontrib><creatorcontrib>Jonczyk, A</creatorcontrib><creatorcontrib>Goodman, S L</creatorcontrib><creatorcontrib>Fox, R I</creatorcontrib><creatorcontrib>Cheresh, D A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Storgard, C M</au><au>Stupack, D G</au><au>Jonczyk, A</au><au>Goodman, S L</au><au>Fox, R I</au><au>Cheresh, D A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decreased angiogenesis and arthritic disease in rabbits treated with an alphavbeta3 antagonist</atitle><jtitle>The Journal of clinical investigation</jtitle><addtitle>J Clin Invest</addtitle><date>1999-01</date><risdate>1999</risdate><volume>103</volume><issue>1</issue><spage>47</spage><epage>54</epage><pages>47-54</pages><issn>0021-9738</issn><abstract>Rheumatoid arthritis (RA) is an inflammatory disease associated with intense angiogenesis and vascular expression of integrin alphavbeta3. Intra-articular administration of a cyclic peptide antagonist of integrin alphavbeta3 to rabbits with antigen-induced arthritis early in disease resulted in inhibition of synovial angiogenesis and reduced synovial cell infiltrate, pannus formation, and cartilage erosions. These effects were not associated with lymphopenia or impairment of leukocyte function. Furthermore, when administered in chronic, preexisting disease, the alphavbeta3 antagonist effectively diminished arthritis severity and was associated with a quantitative increase in apoptosis of the angiogenic blood vessels. Therefore, angiogenesis appears to be a central factor in the initiation and persistence of arthritic disease, and antagonists of integrin alphavbeta3 may represent a novel therapeutic strategy for RA.</abstract><cop>United States</cop><pmid>9884333</pmid><tpages>8</tpages></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Apoptosis - drug effects Arthritis - drug therapy Arthritis - physiopathology Cartilage - drug effects Cartilage - pathology Cell Movement - drug effects Fibroblast Growth Factor 2 - pharmacology Fluorescent Antibody Technique Immunohistochemistry In Situ Nick-End Labeling Leukocytes - drug effects Neovascularization, Pathologic - drug therapy Oligopeptides - physiology Oligopeptides - therapeutic use Peptides, Cyclic - pharmacology Peptides, Cyclic - therapeutic use Rabbits Receptors, Vitronectin - antagonists & inhibitors Receptors, Vitronectin - metabolism Synovial Membrane - drug effects Synovial Membrane - pathology |
| title | Decreased angiogenesis and arthritic disease in rabbits treated with an alphavbeta3 antagonist |
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