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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Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 282; no. 2; pp. H547 - H555
Main Authors Meij, Johanna T. A, Sheikh, Farah, Jimenez, Sarah K, Nickerson, Peter W, Kardami, Elissavet, Cattini, Peter A
Format Journal Article
LanguageEnglish
Published United States 01.02.2002
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
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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
AbstractList 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-CD3epsilon 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.
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
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-CD3ε 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.
Author Meij, Johanna T. A
Cattini, Peter A
Kardami, Elissavet
Jimenez, Sarah K
Sheikh, Farah
Nickerson, Peter W
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Snippet Departments of 1  Physiology, 2  Internal Medicine and Immunology, and 3  Human Anatomy and Cell Science, University of Manitoba, Winnipeg R3E 3J7; and 4...
Fibroblast growth factor-2 (FGF-2) is cardioprotective when added exogenously, stimulates cardiac myocyte proliferation, and is a mediator of tissue repair...
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StartPage H547
SubjectTerms 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
URI http://ajpheart.physiology.org/cgi/content/abstract/282/2/H547
https://www.ncbi.nlm.nih.gov/pubmed/11788402
Volume 282
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