Myocarditis induced by targeted expression of the MCP-1 gene in murine cardiac muscle
To explore the possible role of monocyte chemotactic protein (MCP-1) in inflammatory diseases of the heart, we expressed the murine MCP-1(JE) gene under the control of the alpha-cardiac myosin heavy chain promoter to attempt to target MCP-1 expression to the adult heart muscle. The five lines of tra...
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| Veröffentlicht in: | The American journal of pathology 1998-01, Vol.152 (1), p.101-111 |
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| creator | Kolattukudy, PE Quach, T Bergese, S Breckenridge, S Hensley, J Altschuld, R Gordillo, G Klenotic, S Orosz, C Parker-Thornburg, J |
| description | To explore the possible role of monocyte chemotactic protein (MCP-1) in inflammatory diseases of the heart, we expressed the murine MCP-1(JE) gene under the control of the alpha-cardiac myosin heavy chain promoter to attempt to target MCP-1 expression to the adult heart muscle. The five lines of transgenic mice thus produced showed targeted expression of MCP-1 transcripts and protein in the adult heart muscle and pulmonary vein but not in skeletal muscle. MCP-1 level in the transgenic hearts increased up to 30 to 45 days of age, and leukocyte infiltration into interstitium between cardiomyocytes increased up to 60 to 75 days. The infiltrate was mainly macrophages but not T cells. The presence of MCP-1 in the transgenic hearts did not induce cytokine production indicative of leukocyte activation. Echocardiographic analysis of 1-year-old mice that express MCP-1 in the myocardium and of age-matched controls revealed cardiac hypertrophy and dilation, increases in left ventricular (LV) mass, and systolic and diastolic left ventricular internal diameters. A significant decline in M-mode shortening fraction showed depressed contractile function. Transgenic hearts were 65% heavier, and histological analysis showed moderate myocarditis, edema, and some fibrosis. Thus, MCP-1 expression in the heart muscle may provide a model to investigate myocarditis and cardiomyopathy. |
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The five lines of transgenic mice thus produced showed targeted expression of MCP-1 transcripts and protein in the adult heart muscle and pulmonary vein but not in skeletal muscle. MCP-1 level in the transgenic hearts increased up to 30 to 45 days of age, and leukocyte infiltration into interstitium between cardiomyocytes increased up to 60 to 75 days. The infiltrate was mainly macrophages but not T cells. The presence of MCP-1 in the transgenic hearts did not induce cytokine production indicative of leukocyte activation. Echocardiographic analysis of 1-year-old mice that express MCP-1 in the myocardium and of age-matched controls revealed cardiac hypertrophy and dilation, increases in left ventricular (LV) mass, and systolic and diastolic left ventricular internal diameters. A significant decline in M-mode shortening fraction showed depressed contractile function. Transgenic hearts were 65% heavier, and histological analysis showed moderate myocarditis, edema, and some fibrosis. Thus, MCP-1 expression in the heart muscle may provide a model to investigate myocarditis and cardiomyopathy.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>PMID: 9422528</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>Bethesda, MD: ASIP</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Chemokine CCL2 - genetics ; Chemokine CCL2 - metabolism ; Cytokines - metabolism ; Echocardiography ; Gene Expression - physiology ; Gene Targeting ; Heart ; Heart - physiology ; Medical sciences ; Mice ; Mice, Transgenic - genetics ; Myocarditis - genetics ; Myocarditis - metabolism ; Myocarditis - pathology ; Myocarditis. Cardiomyopathies ; Myocardium - metabolism ; Myocardium - pathology ; RNA - metabolism ; Tissue Distribution</subject><ispartof>The American journal of pathology, 1998-01, Vol.152 (1), p.101-111</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright American Society for Investigative Pathology Jan 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1858131/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1858131/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,729,782,786,887,4026,53798,53800</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2101807$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9422528$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kolattukudy, PE</creatorcontrib><creatorcontrib>Quach, T</creatorcontrib><creatorcontrib>Bergese, S</creatorcontrib><creatorcontrib>Breckenridge, S</creatorcontrib><creatorcontrib>Hensley, J</creatorcontrib><creatorcontrib>Altschuld, R</creatorcontrib><creatorcontrib>Gordillo, G</creatorcontrib><creatorcontrib>Klenotic, S</creatorcontrib><creatorcontrib>Orosz, C</creatorcontrib><creatorcontrib>Parker-Thornburg, J</creatorcontrib><title>Myocarditis induced by targeted expression of the MCP-1 gene in murine cardiac muscle</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>To explore the possible role of monocyte chemotactic protein (MCP-1) in inflammatory diseases of the heart, we expressed the murine MCP-1(JE) gene under the control of the alpha-cardiac myosin heavy chain promoter to attempt to target MCP-1 expression to the adult heart muscle. The five lines of transgenic mice thus produced showed targeted expression of MCP-1 transcripts and protein in the adult heart muscle and pulmonary vein but not in skeletal muscle. MCP-1 level in the transgenic hearts increased up to 30 to 45 days of age, and leukocyte infiltration into interstitium between cardiomyocytes increased up to 60 to 75 days. The infiltrate was mainly macrophages but not T cells. The presence of MCP-1 in the transgenic hearts did not induce cytokine production indicative of leukocyte activation. Echocardiographic analysis of 1-year-old mice that express MCP-1 in the myocardium and of age-matched controls revealed cardiac hypertrophy and dilation, increases in left ventricular (LV) mass, and systolic and diastolic left ventricular internal diameters. A significant decline in M-mode shortening fraction showed depressed contractile function. Transgenic hearts were 65% heavier, and histological analysis showed moderate myocarditis, edema, and some fibrosis. Thus, MCP-1 expression in the heart muscle may provide a model to investigate myocarditis and cardiomyopathy.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Cytokines - metabolism</subject><subject>Echocardiography</subject><subject>Gene Expression - physiology</subject><subject>Gene Targeting</subject><subject>Heart</subject><subject>Heart - physiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Transgenic - genetics</subject><subject>Myocarditis - genetics</subject><subject>Myocarditis - metabolism</subject><subject>Myocarditis - pathology</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>RNA - metabolism</subject><subject>Tissue Distribution</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</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>eNpdkVtLxDAQhYsoul5-glBEfCvk2iQvgizeYBd90OeQptNtll7WpFX33xt1WS9PM8P55nAm2UkmmBOeEazwbjJBCJFMMYYOksMQlnHMqUT7yb5ihHAiJ8nzfN1b40s3uJC6rhwtlGmxTgfjFzDEHt5XHkJwfZf2VTrUkM6njxlOF9BBXEjb0bvYfXkYG8dgGzhO9irTBDjZ1KPk-eb6aXqXzR5u76dXs6ymTA4ZUGsFgooxbhXhJc-FEFZgigqLWGWVkEoWhkamzCWYiipqASMkC8ELWtCj5PLbdzUWLZQWusGbRq-8a41f6944_VfpXK0X_avGkktMcTS42Bj4_mWEMOjWBQtNYzrox6CFyinj-Sd49g9c9qPv4nGaYKmYYIhH6PR3nG2OzWtH_Xyjm2BNU3nTWRe2GMEISyR-QtVuUb85Dzq0pmmiKdZmuYofrLGOLP0A0KqWPg</recordid><startdate>19980101</startdate><enddate>19980101</enddate><creator>Kolattukudy, PE</creator><creator>Quach, T</creator><creator>Bergese, S</creator><creator>Breckenridge, S</creator><creator>Hensley, J</creator><creator>Altschuld, R</creator><creator>Gordillo, G</creator><creator>Klenotic, S</creator><creator>Orosz, C</creator><creator>Parker-Thornburg, J</creator><general>ASIP</general><general>American Society for Investigative Pathology</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8C1</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>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19980101</creationdate><title>Myocarditis induced by targeted expression of the MCP-1 gene in murine cardiac muscle</title><author>Kolattukudy, PE ; Quach, T ; Bergese, S ; Breckenridge, S ; Hensley, J ; Altschuld, R ; Gordillo, G ; Klenotic, S ; Orosz, C ; Parker-Thornburg, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h348t-e3cc70ef445c925d56777c7130bc04fc97898ba370ed68eaf393ce1008b75b3b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Chemokine CCL2 - genetics</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Cytokines - metabolism</topic><topic>Echocardiography</topic><topic>Gene Expression - physiology</topic><topic>Gene Targeting</topic><topic>Heart</topic><topic>Heart - physiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Transgenic - genetics</topic><topic>Myocarditis - genetics</topic><topic>Myocarditis - metabolism</topic><topic>Myocarditis - pathology</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>RNA - metabolism</topic><topic>Tissue Distribution</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kolattukudy, PE</creatorcontrib><creatorcontrib>Quach, T</creatorcontrib><creatorcontrib>Bergese, S</creatorcontrib><creatorcontrib>Breckenridge, S</creatorcontrib><creatorcontrib>Hensley, J</creatorcontrib><creatorcontrib>Altschuld, R</creatorcontrib><creatorcontrib>Gordillo, G</creatorcontrib><creatorcontrib>Klenotic, S</creatorcontrib><creatorcontrib>Orosz, C</creatorcontrib><creatorcontrib>Parker-Thornburg, J</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Public Health 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</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Science Database</collection><collection>Biological Science Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The American journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kolattukudy, PE</au><au>Quach, T</au><au>Bergese, S</au><au>Breckenridge, S</au><au>Hensley, J</au><au>Altschuld, R</au><au>Gordillo, G</au><au>Klenotic, S</au><au>Orosz, C</au><au>Parker-Thornburg, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocarditis induced by targeted expression of the MCP-1 gene in murine cardiac muscle</atitle><jtitle>The American journal of pathology</jtitle><addtitle>Am J Pathol</addtitle><date>1998-01-01</date><risdate>1998</risdate><volume>152</volume><issue>1</issue><spage>101</spage><epage>111</epage><pages>101-111</pages><issn>0002-9440</issn><eissn>1525-2191</eissn><coden>AJPAA4</coden><abstract>To explore the possible role of monocyte chemotactic protein (MCP-1) in inflammatory diseases of the heart, we expressed the murine MCP-1(JE) gene under the control of the alpha-cardiac myosin heavy chain promoter to attempt to target MCP-1 expression to the adult heart muscle. The five lines of transgenic mice thus produced showed targeted expression of MCP-1 transcripts and protein in the adult heart muscle and pulmonary vein but not in skeletal muscle. MCP-1 level in the transgenic hearts increased up to 30 to 45 days of age, and leukocyte infiltration into interstitium between cardiomyocytes increased up to 60 to 75 days. The infiltrate was mainly macrophages but not T cells. The presence of MCP-1 in the transgenic hearts did not induce cytokine production indicative of leukocyte activation. Echocardiographic analysis of 1-year-old mice that express MCP-1 in the myocardium and of age-matched controls revealed cardiac hypertrophy and dilation, increases in left ventricular (LV) mass, and systolic and diastolic left ventricular internal diameters. A significant decline in M-mode shortening fraction showed depressed contractile function. Transgenic hearts were 65% heavier, and histological analysis showed moderate myocarditis, edema, and some fibrosis. Thus, MCP-1 expression in the heart muscle may provide a model to investigate myocarditis and cardiomyopathy.</abstract><cop>Bethesda, MD</cop><pub>ASIP</pub><pmid>9422528</pmid><tpages>11</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Cardiology. Vascular system Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Cytokines - metabolism Echocardiography Gene Expression - physiology Gene Targeting Heart Heart - physiology Medical sciences Mice Mice, Transgenic - genetics Myocarditis - genetics Myocarditis - metabolism Myocarditis - pathology Myocarditis. Cardiomyopathies Myocardium - metabolism Myocardium - pathology RNA - metabolism Tissue Distribution |
| title | Myocarditis induced by targeted expression of the MCP-1 gene in murine cardiac muscle |
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