Hepatocyte Growth Factor Ameliorates the Progression of Experimental Autoimmune Myocarditis: A Potential Role for Induction of T Helper 2 Cytokines
Hepatocyte growth factor (HGF) plays a role in cell protection, antiapoptosis, antifibrosis, and angiogenesis. However, the role of HGF in the immune system is not well defined. We examined the influence of HGF on T cells and the effects of HGF therapy in acute myocarditis. Lewis rats were immunized...
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| Veröffentlicht in: | Circulation research 2005-04, Vol.96 (8), p.823-830 |
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| creator | Futamatsu, Hideki Suzuki, Jun-ichi Mizuno, Shinya Koga, Noritaka Adachi, Susumu Kosuge, Hisanori Maejima, Yasuhiro Hirao, Kenzo Nakamura, Toshikazu Isobe, Mitsuaki |
| description | Hepatocyte growth factor (HGF) plays a role in cell protection, antiapoptosis, antifibrosis, and angiogenesis. However, the role of HGF in the immune system is not well defined. We examined the influence of HGF on T cells and the effects of HGF therapy in acute myocarditis. Lewis rats were immunized on day 0 with cardiac myosin to establish experimental autoimmune myocarditis (EAM). Human HGF gene with hemagglutinating virus of the Japan-envelope vector was injected directly into the myocardium on day 0 or on day 14 (two groups of treated rats). Rats were killed on day 21. Expression of c-Met/HGF receptor in splenocytes and myocardial infiltrating cells was confirmed by immunohistochemical staining or FACS analysis. Myocarditis-affected areas were smaller in the treated rats than in control rats. Cardiac function in the treated rats was markedly improved. An antigen-specific T cell proliferation assay was done with CD4-positive T cells isolated from control rats stimulated with cardiac myosin. HGF suppressed T cell proliferation and production of IFN-γ and increased production of IL-4 and IL-10 secreted from CD4-positive T cells in vitro. Additionally, TUNEL assay revealed that HGF reduced apoptosis in cardiomyocytes. HGF reduced the severity of EAM by inducing T helper 2 cytokines and suppressing apoptosis of cardiomyocytes. HGF has potential as a new therapy for myocarditis. |
| doi_str_mv | 10.1161/01.RES.0000163016.52653.2e |
| format | Article |
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However, the role of HGF in the immune system is not well defined. We examined the influence of HGF on T cells and the effects of HGF therapy in acute myocarditis. Lewis rats were immunized on day 0 with cardiac myosin to establish experimental autoimmune myocarditis (EAM). Human HGF gene with hemagglutinating virus of the Japan-envelope vector was injected directly into the myocardium on day 0 or on day 14 (two groups of treated rats). Rats were killed on day 21. Expression of c-Met/HGF receptor in splenocytes and myocardial infiltrating cells was confirmed by immunohistochemical staining or FACS analysis. Myocarditis-affected areas were smaller in the treated rats than in control rats. Cardiac function in the treated rats was markedly improved. An antigen-specific T cell proliferation assay was done with CD4-positive T cells isolated from control rats stimulated with cardiac myosin. HGF suppressed T cell proliferation and production of IFN-γ and increased production of IL-4 and IL-10 secreted from CD4-positive T cells in vitro. Additionally, TUNEL assay revealed that HGF reduced apoptosis in cardiomyocytes. HGF reduced the severity of EAM by inducing T helper 2 cytokines and suppressing apoptosis of cardiomyocytes. HGF has potential as a new therapy for myocarditis.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.0000163016.52653.2e</identifier><identifier>PMID: 15774858</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Apoptosis ; Autoimmune Diseases - immunology ; Autoimmune Diseases - therapy ; Biological and medical sciences ; Cardiology. Vascular system ; Cytokines - biosynthesis ; Fundamental and applied biological sciences. Psychology ; Genetic Therapy ; Heart ; Hepatocyte Growth Factor - genetics ; Hepatocyte Growth Factor - physiology ; Lymphocyte Activation ; Male ; Medical sciences ; Myocarditis - immunology ; Myocarditis - therapy ; Myocarditis. Cardiomyopathies ; Proto-Oncogene Proteins c-met - analysis ; Rats ; Rats, Inbred Lew ; Th2 Cells - immunology ; Transfection ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 2005-04, Vol.96 (8), p.823-830</ispartof><rights>2005 American Heart Association, Inc.</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4025-9efc02cea51de1de859974fa2219ec6378e3634ff4b1681eb3b25977f395759d3</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=16763463$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15774858$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Futamatsu, Hideki</creatorcontrib><creatorcontrib>Suzuki, Jun-ichi</creatorcontrib><creatorcontrib>Mizuno, Shinya</creatorcontrib><creatorcontrib>Koga, Noritaka</creatorcontrib><creatorcontrib>Adachi, Susumu</creatorcontrib><creatorcontrib>Kosuge, Hisanori</creatorcontrib><creatorcontrib>Maejima, Yasuhiro</creatorcontrib><creatorcontrib>Hirao, Kenzo</creatorcontrib><creatorcontrib>Nakamura, Toshikazu</creatorcontrib><creatorcontrib>Isobe, Mitsuaki</creatorcontrib><title>Hepatocyte Growth Factor Ameliorates the Progression of Experimental Autoimmune Myocarditis: A Potential Role for Induction of T Helper 2 Cytokines</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Hepatocyte growth factor (HGF) plays a role in cell protection, antiapoptosis, antifibrosis, and angiogenesis. However, the role of HGF in the immune system is not well defined. We examined the influence of HGF on T cells and the effects of HGF therapy in acute myocarditis. Lewis rats were immunized on day 0 with cardiac myosin to establish experimental autoimmune myocarditis (EAM). Human HGF gene with hemagglutinating virus of the Japan-envelope vector was injected directly into the myocardium on day 0 or on day 14 (two groups of treated rats). Rats were killed on day 21. Expression of c-Met/HGF receptor in splenocytes and myocardial infiltrating cells was confirmed by immunohistochemical staining or FACS analysis. Myocarditis-affected areas were smaller in the treated rats than in control rats. Cardiac function in the treated rats was markedly improved. An antigen-specific T cell proliferation assay was done with CD4-positive T cells isolated from control rats stimulated with cardiac myosin. HGF suppressed T cell proliferation and production of IFN-γ and increased production of IL-4 and IL-10 secreted from CD4-positive T cells in vitro. Additionally, TUNEL assay revealed that HGF reduced apoptosis in cardiomyocytes. HGF reduced the severity of EAM by inducing T helper 2 cytokines and suppressing apoptosis of cardiomyocytes. HGF has potential as a new therapy for myocarditis.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - therapy</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cytokines - biosynthesis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic Therapy</subject><subject>Heart</subject><subject>Hepatocyte Growth Factor - genetics</subject><subject>Hepatocyte Growth Factor - physiology</subject><subject>Lymphocyte Activation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocarditis - immunology</subject><subject>Myocarditis - therapy</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Proto-Oncogene Proteins c-met - analysis</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Th2 Cells - immunology</subject><subject>Transfection</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkd9q2zAUxs3YWNNurzDEYL2zp79W1LsQ0qbQsdJ110KRjxevspVJMlmeYy9ctTHkckJCcPid79PRVxSfCa4IqclXTKqH1Y8K50Vqlk8laC1YReFNMSOC8pILSd4WswyoUjKGz4rzGH9nnDOq3hdnREjJ52I-K_6tYWeSt4cE6Cb4fdqia2OTD2jRg-t8MAkiSltA98H_ChBj5wfkW7T6u4PQ9TAk49BiTL7r-3EA9O3grQlNl7p4hRbo3qeMdJl58A5Qm4Vvh2a0aZJ5RGtwWQlRtDwk_9QNED8U71rjInyc7ovi5_Xqcbku777f3C4Xd6XlmIpSQWsxtWAEaSDvuVBK8tZQShTYmsk5sJrxtuUbUs8JbNiGCiVly5SQQjXsorg86u6C_zNCTLrvogXnzAB-jLqWUnEm8X9BIhmnitAMXh1BG3yMAVq9y39kwkETrF-y05jonJ0-Zadfs9MUcvOnyWXc9NCcWqewMvBlAky0xrXBDLaLJ66WedyaZY4fub13CUJ8cuMegt6CcWn7ap2NaUkxFji_G5cvJcGeASPbs8o</recordid><startdate>20050429</startdate><enddate>20050429</enddate><creator>Futamatsu, Hideki</creator><creator>Suzuki, Jun-ichi</creator><creator>Mizuno, Shinya</creator><creator>Koga, Noritaka</creator><creator>Adachi, Susumu</creator><creator>Kosuge, Hisanori</creator><creator>Maejima, Yasuhiro</creator><creator>Hirao, Kenzo</creator><creator>Nakamura, Toshikazu</creator><creator>Isobe, Mitsuaki</creator><general>American Heart Association, Inc</general><general>Lippincott</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20050429</creationdate><title>Hepatocyte Growth Factor Ameliorates the Progression of Experimental Autoimmune Myocarditis: A Potential Role for Induction of T Helper 2 Cytokines</title><author>Futamatsu, Hideki ; Suzuki, Jun-ichi ; Mizuno, Shinya ; Koga, Noritaka ; Adachi, Susumu ; Kosuge, Hisanori ; Maejima, Yasuhiro ; Hirao, Kenzo ; Nakamura, Toshikazu ; Isobe, Mitsuaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4025-9efc02cea51de1de859974fa2219ec6378e3634ff4b1681eb3b25977f395759d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Autoimmune Diseases - immunology</topic><topic>Autoimmune Diseases - therapy</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cytokines - biosynthesis</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic Therapy</topic><topic>Heart</topic><topic>Hepatocyte Growth Factor - genetics</topic><topic>Hepatocyte Growth Factor - physiology</topic><topic>Lymphocyte Activation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocarditis - immunology</topic><topic>Myocarditis - therapy</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Proto-Oncogene Proteins c-met - analysis</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Th2 Cells - immunology</topic><topic>Transfection</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Futamatsu, Hideki</creatorcontrib><creatorcontrib>Suzuki, Jun-ichi</creatorcontrib><creatorcontrib>Mizuno, Shinya</creatorcontrib><creatorcontrib>Koga, Noritaka</creatorcontrib><creatorcontrib>Adachi, Susumu</creatorcontrib><creatorcontrib>Kosuge, Hisanori</creatorcontrib><creatorcontrib>Maejima, Yasuhiro</creatorcontrib><creatorcontrib>Hirao, Kenzo</creatorcontrib><creatorcontrib>Nakamura, Toshikazu</creatorcontrib><creatorcontrib>Isobe, Mitsuaki</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Futamatsu, Hideki</au><au>Suzuki, Jun-ichi</au><au>Mizuno, Shinya</au><au>Koga, Noritaka</au><au>Adachi, Susumu</au><au>Kosuge, Hisanori</au><au>Maejima, Yasuhiro</au><au>Hirao, Kenzo</au><au>Nakamura, Toshikazu</au><au>Isobe, Mitsuaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatocyte Growth Factor Ameliorates the Progression of Experimental Autoimmune Myocarditis: A Potential Role for Induction of T Helper 2 Cytokines</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2005-04-29</date><risdate>2005</risdate><volume>96</volume><issue>8</issue><spage>823</spage><epage>830</epage><pages>823-830</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>Hepatocyte growth factor (HGF) plays a role in cell protection, antiapoptosis, antifibrosis, and angiogenesis. However, the role of HGF in the immune system is not well defined. We examined the influence of HGF on T cells and the effects of HGF therapy in acute myocarditis. Lewis rats were immunized on day 0 with cardiac myosin to establish experimental autoimmune myocarditis (EAM). Human HGF gene with hemagglutinating virus of the Japan-envelope vector was injected directly into the myocardium on day 0 or on day 14 (two groups of treated rats). Rats were killed on day 21. Expression of c-Met/HGF receptor in splenocytes and myocardial infiltrating cells was confirmed by immunohistochemical staining or FACS analysis. Myocarditis-affected areas were smaller in the treated rats than in control rats. Cardiac function in the treated rats was markedly improved. An antigen-specific T cell proliferation assay was done with CD4-positive T cells isolated from control rats stimulated with cardiac myosin. HGF suppressed T cell proliferation and production of IFN-γ and increased production of IL-4 and IL-10 secreted from CD4-positive T cells in vitro. Additionally, TUNEL assay revealed that HGF reduced apoptosis in cardiomyocytes. HGF reduced the severity of EAM by inducing T helper 2 cytokines and suppressing apoptosis of cardiomyocytes. HGF has potential as a new therapy for myocarditis.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>15774858</pmid><doi>10.1161/01.RES.0000163016.52653.2e</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Apoptosis Autoimmune Diseases - immunology Autoimmune Diseases - therapy Biological and medical sciences Cardiology. Vascular system Cytokines - biosynthesis Fundamental and applied biological sciences. Psychology Genetic Therapy Heart Hepatocyte Growth Factor - genetics Hepatocyte Growth Factor - physiology Lymphocyte Activation Male Medical sciences Myocarditis - immunology Myocarditis - therapy Myocarditis. Cardiomyopathies Proto-Oncogene Proteins c-met - analysis Rats Rats, Inbred Lew Th2 Cells - immunology Transfection Vertebrates: cardiovascular system |
| title | Hepatocyte Growth Factor Ameliorates the Progression of Experimental Autoimmune Myocarditis: A Potential Role for Induction of T Helper 2 Cytokines |
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