Exacerbation of myocardial injury in transgenic mice overexpressing FGF-2 is T cell dependent
Departments of 1 Physiology, 2 Internal Medicine and Immunology, and 3 Human Anatomy and Cell Science, University of Manitoba, Winnipeg R3E 3J7; and 4 Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada R2H 2A6 Fibroblast growth factor-2 (FGF-2...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2002-02, Vol.282 (2), p.H547-H555 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 282 |
| creator | Meij, Johanna T. A Sheikh, Farah Jimenez, Sarah K Nickerson, Peter W Kardami, Elissavet Cattini, Peter A |
| description | Departments of 1 Physiology, 2 Internal Medicine and
Immunology, and 3 Human Anatomy and Cell Science, University
of Manitoba, Winnipeg R3E 3J7; and 4 Institute of Cardiovascular
Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba,
Canada R2H 2A6
Fibroblast growth factor-2 (FGF-2) is
cardioprotective when added exogenously, stimulates cardiac myocyte
proliferation, and is a mediator of tissue repair after injury.
Furthermore, transgenic (TG) mice overexpressing FGF-2 in cardiac
muscle demonstrate increased resistance to injury in an isolated heart
model of ischemia-reperfusion. We investigated how increasing
the endogenous FGF-2 levels in the heart affects the extent of
myocardial damage induced by isoproterenol in vivo. Histopathological
evaluation of hearts after intraperitoneal injection of isoproterenol
yielded significantly higher scores for myocardial damage in FGF-2 TG
lines compared with non-TG mice. After 1 day, FGF-2 TG mouse hearts
displayed more cellular infiltration correlating with increased tissue
damage. Immunostaining of non-TG and FGF-2 TG mouse hearts showed the
presence of leukocytes in the infiltrate, including T cells expressing
FGF receptor-1. Treatment of mice with T cell suppressors cyclosporin A
and anti-CD3 significantly decreased the level of myocardial injury
observed after isoproterenol and equalized the histopathology scores in
FGF-2 TG and non-TG hearts. These data demonstrate a direct T cell
involvement in the response to isoproterenol-induced injury in vivo.
Moreover, the findings indicate that the exacerbation of myocardial
damage in FGF-2 TG mice was dependent on T cell infiltration,
implicating FGF-2 in the inflammatory response seen in cardiac tissue
after injury in vivo.
myocardium; lymphocytes |
| doi_str_mv | 10.1152/ajpheart.01019.2000 |
| format | Article |
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Immunology, and 3 Human Anatomy and Cell Science, University
of Manitoba, Winnipeg R3E 3J7; and 4 Institute of Cardiovascular
Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba,
Canada R2H 2A6
Fibroblast growth factor-2 (FGF-2) is
cardioprotective when added exogenously, stimulates cardiac myocyte
proliferation, and is a mediator of tissue repair after injury.
Furthermore, transgenic (TG) mice overexpressing FGF-2 in cardiac
muscle demonstrate increased resistance to injury in an isolated heart
model of ischemia-reperfusion. We investigated how increasing
the endogenous FGF-2 levels in the heart affects the extent of
myocardial damage induced by isoproterenol in vivo. Histopathological
evaluation of hearts after intraperitoneal injection of isoproterenol
yielded significantly higher scores for myocardial damage in FGF-2 TG
lines compared with non-TG mice. After 1 day, FGF-2 TG mouse hearts
displayed more cellular infiltration correlating with increased tissue
damage. Immunostaining of non-TG and FGF-2 TG mouse hearts showed the
presence of leukocytes in the infiltrate, including T cells expressing
FGF receptor-1. Treatment of mice with T cell suppressors cyclosporin A
and anti-CD3 significantly decreased the level of myocardial injury
observed after isoproterenol and equalized the histopathology scores in
FGF-2 TG and non-TG hearts. These data demonstrate a direct T cell
involvement in the response to isoproterenol-induced injury in vivo.
Moreover, the findings indicate that the exacerbation of myocardial
damage in FGF-2 TG mice was dependent on T cell infiltration,
implicating FGF-2 in the inflammatory response seen in cardiac tissue
after injury in vivo.
myocardium; lymphocytes</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.01019.2000</identifier><identifier>PMID: 11788402</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antibodies, Monoclonal - pharmacology ; CD3 Complex ; Cyclosporine - pharmacology ; Female ; Fibroblast Growth Factor 2 - genetics ; Fibroblast Growth Factor 2 - immunology ; Gene Expression - immunology ; Heart Diseases - chemically induced ; Heart Diseases - drug therapy ; Heart Diseases - immunology ; Immunosuppressive Agents - pharmacology ; Isoproterenol ; Male ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; Myocardium - immunology ; Myocardium - pathology ; Receptors, Antigen, T-Cell - immunology ; Sympathomimetics ; T-Lymphocytes - immunology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2002-02, Vol.282 (2), p.H547-H555</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-f7e491c2a978185c97ce50b743286d10e41d2b5ad827e18fe6d47d5ee5d0fbf3</citedby><cites>FETCH-LOGICAL-c391t-f7e491c2a978185c97ce50b743286d10e41d2b5ad827e18fe6d47d5ee5d0fbf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11788402$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Meij, Johanna T. A</creatorcontrib><creatorcontrib>Sheikh, Farah</creatorcontrib><creatorcontrib>Jimenez, Sarah K</creatorcontrib><creatorcontrib>Nickerson, Peter W</creatorcontrib><creatorcontrib>Kardami, Elissavet</creatorcontrib><creatorcontrib>Cattini, Peter A</creatorcontrib><title>Exacerbation of myocardial injury in transgenic mice overexpressing FGF-2 is T cell dependent</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Departments of 1 Physiology, 2 Internal Medicine and
Immunology, and 3 Human Anatomy and Cell Science, University
of Manitoba, Winnipeg R3E 3J7; and 4 Institute of Cardiovascular
Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba,
Canada R2H 2A6
Fibroblast growth factor-2 (FGF-2) is
cardioprotective when added exogenously, stimulates cardiac myocyte
proliferation, and is a mediator of tissue repair after injury.
Furthermore, transgenic (TG) mice overexpressing FGF-2 in cardiac
muscle demonstrate increased resistance to injury in an isolated heart
model of ischemia-reperfusion. We investigated how increasing
the endogenous FGF-2 levels in the heart affects the extent of
myocardial damage induced by isoproterenol in vivo. Histopathological
evaluation of hearts after intraperitoneal injection of isoproterenol
yielded significantly higher scores for myocardial damage in FGF-2 TG
lines compared with non-TG mice. After 1 day, FGF-2 TG mouse hearts
displayed more cellular infiltration correlating with increased tissue
damage. Immunostaining of non-TG and FGF-2 TG mouse hearts showed the
presence of leukocytes in the infiltrate, including T cells expressing
FGF receptor-1. Treatment of mice with T cell suppressors cyclosporin A
and anti-CD3 significantly decreased the level of myocardial injury
observed after isoproterenol and equalized the histopathology scores in
FGF-2 TG and non-TG hearts. These data demonstrate a direct T cell
involvement in the response to isoproterenol-induced injury in vivo.
Moreover, the findings indicate that the exacerbation of myocardial
damage in FGF-2 TG mice was dependent on T cell infiltration,
implicating FGF-2 in the inflammatory response seen in cardiac tissue
after injury in vivo.
myocardium; lymphocytes</description><subject>Animals</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>CD3 Complex</subject><subject>Cyclosporine - pharmacology</subject><subject>Female</subject><subject>Fibroblast Growth Factor 2 - genetics</subject><subject>Fibroblast Growth Factor 2 - immunology</subject><subject>Gene Expression - immunology</subject><subject>Heart Diseases - chemically induced</subject><subject>Heart Diseases - drug therapy</subject><subject>Heart Diseases - immunology</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Isoproterenol</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Transgenic</subject><subject>Myocardium - immunology</subject><subject>Myocardium - pathology</subject><subject>Receptors, Antigen, T-Cell - immunology</subject><subject>Sympathomimetics</subject><subject>T-Lymphocytes - immunology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtOwzAURC0EoqXwBUjIP5DiRxwn7FDVB1IlNt0iy7FvWldpEtkpNH9PSgtdsZrFzJnFQeiRkjGlgj3rbbMB7dsxoYRmY0YIuULDvmERFTy7RkPCEx4llIsBugth2w-ETPgtGlAq0zQmbIg-pgdtwOe6dXWF6wLvutpob50usau2e9_1gVuvq7CGyhm8cwZw_QkeDo2HEFy1xrP5LGLYBbzCBsoSW2igslC19-im0GWAh3OO0Go2XU0W0fJ9_jZ5XUaGZ7SNCglxRg3TmUxpKkwmDQiSy5izNLGUQEwty4W2KZNA0wISG0srAIQlRV7wEeKnW-PrEDwUqvFup32nKFFHV-rXlfpxpY6ueurpRDX7fAf2wpzl9IPxabBx682X86CaTRdcXdbr7vLIUqaYWohY9sDL_8BsX5YrOLR_5AVUjS34NzksjlM</recordid><startdate>20020201</startdate><enddate>20020201</enddate><creator>Meij, Johanna T. A</creator><creator>Sheikh, Farah</creator><creator>Jimenez, Sarah K</creator><creator>Nickerson, Peter W</creator><creator>Kardami, Elissavet</creator><creator>Cattini, Peter A</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20020201</creationdate><title>Exacerbation of myocardial injury in transgenic mice overexpressing FGF-2 is T cell dependent</title><author>Meij, Johanna T. A ; Sheikh, Farah ; Jimenez, Sarah K ; Nickerson, Peter W ; Kardami, Elissavet ; Cattini, Peter A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-f7e491c2a978185c97ce50b743286d10e41d2b5ad827e18fe6d47d5ee5d0fbf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>CD3 Complex</topic><topic>Cyclosporine - pharmacology</topic><topic>Female</topic><topic>Fibroblast Growth Factor 2 - genetics</topic><topic>Fibroblast Growth Factor 2 - immunology</topic><topic>Gene Expression - immunology</topic><topic>Heart Diseases - chemically induced</topic><topic>Heart Diseases - drug therapy</topic><topic>Heart Diseases - immunology</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Isoproterenol</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Transgenic</topic><topic>Myocardium - immunology</topic><topic>Myocardium - pathology</topic><topic>Receptors, Antigen, T-Cell - immunology</topic><topic>Sympathomimetics</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meij, Johanna T. A</creatorcontrib><creatorcontrib>Sheikh, Farah</creatorcontrib><creatorcontrib>Jimenez, Sarah K</creatorcontrib><creatorcontrib>Nickerson, Peter W</creatorcontrib><creatorcontrib>Kardami, Elissavet</creatorcontrib><creatorcontrib>Cattini, Peter A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Meij, Johanna T. A</au><au>Sheikh, Farah</au><au>Jimenez, Sarah K</au><au>Nickerson, Peter W</au><au>Kardami, Elissavet</au><au>Cattini, Peter A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exacerbation of myocardial injury in transgenic mice overexpressing FGF-2 is T cell dependent</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2002-02-01</date><risdate>2002</risdate><volume>282</volume><issue>2</issue><spage>H547</spage><epage>H555</epage><pages>H547-H555</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Departments of 1 Physiology, 2 Internal Medicine and
Immunology, and 3 Human Anatomy and Cell Science, University
of Manitoba, Winnipeg R3E 3J7; and 4 Institute of Cardiovascular
Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba,
Canada R2H 2A6
Fibroblast growth factor-2 (FGF-2) is
cardioprotective when added exogenously, stimulates cardiac myocyte
proliferation, and is a mediator of tissue repair after injury.
Furthermore, transgenic (TG) mice overexpressing FGF-2 in cardiac
muscle demonstrate increased resistance to injury in an isolated heart
model of ischemia-reperfusion. We investigated how increasing
the endogenous FGF-2 levels in the heart affects the extent of
myocardial damage induced by isoproterenol in vivo. Histopathological
evaluation of hearts after intraperitoneal injection of isoproterenol
yielded significantly higher scores for myocardial damage in FGF-2 TG
lines compared with non-TG mice. After 1 day, FGF-2 TG mouse hearts
displayed more cellular infiltration correlating with increased tissue
damage. Immunostaining of non-TG and FGF-2 TG mouse hearts showed the
presence of leukocytes in the infiltrate, including T cells expressing
FGF receptor-1. Treatment of mice with T cell suppressors cyclosporin A
and anti-CD3 significantly decreased the level of myocardial injury
observed after isoproterenol and equalized the histopathology scores in
FGF-2 TG and non-TG hearts. These data demonstrate a direct T cell
involvement in the response to isoproterenol-induced injury in vivo.
Moreover, the findings indicate that the exacerbation of myocardial
damage in FGF-2 TG mice was dependent on T cell infiltration,
implicating FGF-2 in the inflammatory response seen in cardiac tissue
after injury in vivo.
myocardium; lymphocytes</abstract><cop>United States</cop><pmid>11788402</pmid><doi>10.1152/ajpheart.01019.2000</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 2002-02, Vol.282 (2), p.H547-H555 |
| issn | 0363-6135 1522-1539 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpheart_282_2_H547 |
| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Antibodies, Monoclonal - pharmacology CD3 Complex Cyclosporine - pharmacology Female Fibroblast Growth Factor 2 - genetics Fibroblast Growth Factor 2 - immunology Gene Expression - immunology Heart Diseases - chemically induced Heart Diseases - drug therapy Heart Diseases - immunology Immunosuppressive Agents - pharmacology Isoproterenol Male Mice Mice, Inbred Strains Mice, Transgenic Myocardium - immunology Myocardium - pathology Receptors, Antigen, T-Cell - immunology Sympathomimetics T-Lymphocytes - immunology |
| title | Exacerbation of myocardial injury in transgenic mice overexpressing FGF-2 is T cell dependent |
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