Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis
Rat adjuvant arthritis is an experimental model widely used to evaluate etiopathogenetic mechanisms in chronic inflammation. We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the...
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| Veröffentlicht in: | Laboratory investigation 2005-01, Vol.85 (1), p.34-44 |
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| creator | Devesa, Isabel Ferrándiz, Maria Luisa Guillén, Isabel Cerdá, José Miguel Alcaraz, Maria José |
| description | Rat adjuvant arthritis is an experimental model widely used to evaluate etiopathogenetic mechanisms in chronic inflammation. We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the upregulation of HO-1, whereas selective inhibition of inducible NO synthase (iNOS) after the onset of arthritis decreased HO-1 expression, suggesting that the induction of this enzyme may depend on NO produced by iNOS. Therapeutic administration of the HO-1 inhibitor tin protoporphyrin IX was able to control the symptoms of arthritis. This agent significantly decreased leukocyte infiltration, hyperplastic synovitis, erosion of articular cartilage and osteolysis, as well as the production of inflammatory mediators. In this experimental model, HO-1 can be involved in vascular endothelial growth factor production and angiogenesis. These results support a role for HO-1 in mediating the progression of the disease in this model of chronic arthritis. |
| doi_str_mv | 10.1038/labinvest.3700205 |
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We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the upregulation of HO-1, whereas selective inhibition of inducible NO synthase (iNOS) after the onset of arthritis decreased HO-1 expression, suggesting that the induction of this enzyme may depend on NO produced by iNOS. Therapeutic administration of the HO-1 inhibitor tin protoporphyrin IX was able to control the symptoms of arthritis. This agent significantly decreased leukocyte infiltration, hyperplastic synovitis, erosion of articular cartilage and osteolysis, as well as the production of inflammatory mediators. In this experimental model, HO-1 can be involved in vascular endothelial growth factor production and angiogenesis. These results support a role for HO-1 in mediating the progression of the disease in this model of chronic arthritis.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.3700205</identifier><identifier>PMID: 15543205</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>Animals ; Arthritis, Experimental - drug therapy ; Arthritis, Experimental - enzymology ; Arthritis, Experimental - pathology ; Biological and medical sciences ; Biotechnology ; chronic inflammation ; Cyclooxygenase 2 ; Disease Models, Animal ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; Heat-Shock Proteins - antagonists & inhibitors ; Heat-Shock Proteins - metabolism ; Heme Oxygenase (Decyclizing) ; Hindlimb - drug effects ; Hindlimb - enzymology ; Hindlimb - pathology ; HO-1 ; iNOS ; Investigative techniques, diagnostic techniques (general aspects) ; Laboratory Medicine ; Lysine - analogs & derivatives ; Lysine - pharmacology ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Oxygenases - antagonists & inhibitors ; Oxygenases - metabolism ; Pathology ; Prostaglandin-Endoperoxide Synthases - metabolism ; Protoporphyrins - pharmacology ; rat adjuvant arthritis ; Rats ; Rats, Inbred Lew ; research-article ; Tumor Necrosis Factor-alpha - metabolism ; Up-Regulation ; Vascular Endothelial Growth Factor A - metabolism ; VEGF</subject><ispartof>Laboratory investigation, 2005-01, Vol.85 (1), p.34-44</ispartof><rights>2005 United States & Canadian Academy of Pathology</rights><rights>United States and Canadian Academy of Pathology, Inc. 2005</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-f1cd8944cd838862b6e201d1dd7f80260ac344f8805f3280f53b8cfa1cdcd34e3</citedby><cites>FETCH-LOGICAL-c516t-f1cd8944cd838862b6e201d1dd7f80260ac344f8805f3280f53b8cfa1cdcd34e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4023,27922,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16525818$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15543205$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Devesa, Isabel</creatorcontrib><creatorcontrib>Ferrándiz, Maria Luisa</creatorcontrib><creatorcontrib>Guillén, Isabel</creatorcontrib><creatorcontrib>Cerdá, José Miguel</creatorcontrib><creatorcontrib>Alcaraz, Maria José</creatorcontrib><title>Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>Rat adjuvant arthritis is an experimental model widely used to evaluate etiopathogenetic mechanisms in chronic inflammation. We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the upregulation of HO-1, whereas selective inhibition of inducible NO synthase (iNOS) after the onset of arthritis decreased HO-1 expression, suggesting that the induction of this enzyme may depend on NO produced by iNOS. Therapeutic administration of the HO-1 inhibitor tin protoporphyrin IX was able to control the symptoms of arthritis. This agent significantly decreased leukocyte infiltration, hyperplastic synovitis, erosion of articular cartilage and osteolysis, as well as the production of inflammatory mediators. In this experimental model, HO-1 can be involved in vascular endothelial growth factor production and angiogenesis. These results support a role for HO-1 in mediating the progression of the disease in this model of chronic arthritis.</description><subject>Animals</subject><subject>Arthritis, Experimental - drug therapy</subject><subject>Arthritis, Experimental - enzymology</subject><subject>Arthritis, Experimental - pathology</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>chronic inflammation</subject><subject>Cyclooxygenase 2</subject><subject>Disease Models, Animal</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heat-Shock Proteins - antagonists & inhibitors</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>Heme Oxygenase (Decyclizing)</subject><subject>Hindlimb - drug effects</subject><subject>Hindlimb - enzymology</subject><subject>Hindlimb - pathology</subject><subject>HO-1</subject><subject>iNOS</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Laboratory Medicine</subject><subject>Lysine - analogs & derivatives</subject><subject>Lysine - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Oxygenases - antagonists & inhibitors</subject><subject>Oxygenases - metabolism</subject><subject>Pathology</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Protoporphyrins - pharmacology</subject><subject>rat adjuvant arthritis</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>research-article</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Up-Regulation</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>VEGF</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kV9LHDEUxUOp1NX2A_RBGQr2bWz-TDIRn0RsFQR9aJ9DNrnZzTKb2CSz6LdvZAYX-uBLbsj9nXMvJwh9JficYCZ_DHrpww5yOWc9xhTzD2hBOMMtZrj_iBb1jbVCsv4QHeW8wZh0neCf0CHhvGOVX6CHx1ggFK-HJsUBmuiaNWxrfX5ZQdAZWtL40JQ1NE8prhLk7GN4xZIujbabcadDvaSyTr74_BkdOD1k-DLXY_Tn583v69v2_uHX3fXVfWs4EaV1xFh50XX1ZFIKuhRAMbHE2t5JTAXWhnWdkxJzx6jEjrOlNE5XmbGsA3aMvk--dau_Y41AbX02MAw6QByzEj1jUvS8gt_-AzdxTKHupijFVF4QxipEJsikmHMCp56S3-r0oghWr1Grt6jVHHXVnM7G43ILdq-Ys63A2QzobPTgkg7G5z0nOOWSyMrRicu1FVaQ9hu-N_1kEgVdxgRvrvv-5dSH-gk7X02z8RAMWJ_AFGWjf8f9Hzi8uAw</recordid><startdate>200501</startdate><enddate>200501</enddate><creator>Devesa, Isabel</creator><creator>Ferrándiz, Maria Luisa</creator><creator>Guillén, Isabel</creator><creator>Cerdá, José Miguel</creator><creator>Alcaraz, Maria José</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200501</creationdate><title>Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis</title><author>Devesa, Isabel ; Ferrándiz, Maria Luisa ; Guillén, Isabel ; Cerdá, José Miguel ; Alcaraz, Maria José</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c516t-f1cd8944cd838862b6e201d1dd7f80260ac344f8805f3280f53b8cfa1cdcd34e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Arthritis, Experimental - drug therapy</topic><topic>Arthritis, Experimental - enzymology</topic><topic>Arthritis, Experimental - pathology</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>chronic inflammation</topic><topic>Cyclooxygenase 2</topic><topic>Disease Models, Animal</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heat-Shock Proteins - antagonists & inhibitors</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>Heme Oxygenase (Decyclizing)</topic><topic>Hindlimb - drug effects</topic><topic>Hindlimb - enzymology</topic><topic>Hindlimb - pathology</topic><topic>HO-1</topic><topic>iNOS</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Laboratory Medicine</topic><topic>Lysine - analogs & derivatives</topic><topic>Lysine - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Oxygenases - antagonists & inhibitors</topic><topic>Oxygenases - metabolism</topic><topic>Pathology</topic><topic>Prostaglandin-Endoperoxide Synthases - metabolism</topic><topic>Protoporphyrins - pharmacology</topic><topic>rat adjuvant arthritis</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>research-article</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Up-Regulation</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>VEGF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Devesa, Isabel</creatorcontrib><creatorcontrib>Ferrándiz, Maria Luisa</creatorcontrib><creatorcontrib>Guillén, Isabel</creatorcontrib><creatorcontrib>Cerdá, José Miguel</creatorcontrib><creatorcontrib>Alcaraz, Maria José</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS 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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Devesa, Isabel</au><au>Ferrándiz, Maria Luisa</au><au>Guillén, Isabel</au><au>Cerdá, José Miguel</au><au>Alcaraz, Maria José</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2005-01</date><risdate>2005</risdate><volume>85</volume><issue>1</issue><spage>34</spage><epage>44</epage><pages>34-44</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><coden>LAINAW</coden><abstract>Rat adjuvant arthritis is an experimental model widely used to evaluate etiopathogenetic mechanisms in chronic inflammation. We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the upregulation of HO-1, whereas selective inhibition of inducible NO synthase (iNOS) after the onset of arthritis decreased HO-1 expression, suggesting that the induction of this enzyme may depend on NO produced by iNOS. Therapeutic administration of the HO-1 inhibitor tin protoporphyrin IX was able to control the symptoms of arthritis. This agent significantly decreased leukocyte infiltration, hyperplastic synovitis, erosion of articular cartilage and osteolysis, as well as the production of inflammatory mediators. In this experimental model, HO-1 can be involved in vascular endothelial growth factor production and angiogenesis. These results support a role for HO-1 in mediating the progression of the disease in this model of chronic arthritis.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>15543205</pmid><doi>10.1038/labinvest.3700205</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arthritis, Experimental - drug therapy Arthritis, Experimental - enzymology Arthritis, Experimental - pathology Biological and medical sciences Biotechnology chronic inflammation Cyclooxygenase 2 Disease Models, Animal Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology Heat-Shock Proteins - antagonists & inhibitors Heat-Shock Proteins - metabolism Heme Oxygenase (Decyclizing) Hindlimb - drug effects Hindlimb - enzymology Hindlimb - pathology HO-1 iNOS Investigative techniques, diagnostic techniques (general aspects) Laboratory Medicine Lysine - analogs & derivatives Lysine - pharmacology Male Medical sciences Medicine Medicine & Public Health Nitric Oxide - metabolism Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Oxygenases - antagonists & inhibitors Oxygenases - metabolism Pathology Prostaglandin-Endoperoxide Synthases - metabolism Protoporphyrins - pharmacology rat adjuvant arthritis Rats Rats, Inbred Lew research-article Tumor Necrosis Factor-alpha - metabolism Up-Regulation Vascular Endothelial Growth Factor A - metabolism VEGF |
| title | Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis |
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