Key result
Overexpression of FGF-2 in transgenic mice exacerbated isoproterenol-induced myocardial damage, an effect that was dependent on T cell infiltration and reversed by T cell suppressors.
Why the study?
Does T cell suppression reduce isoproterenol-induced myocardial injury in FGF-2 transgenic mice?
Does T cell suppression reduce isoproterenol-induced myocardial injury in FGF-2 transgenic mice?
Exacerbation of myocardial damage in FGF-2 transgenic mice after isoproterenol injury is dependent on T cell infiltration, highlighting a role for FGF-2 in the inflammatory response.
Answers are grounded in this paper and cite their sources.
T cell suppression mitigates FGF-2-exacerbated injury in this mouse model; hypothesis-generating for immunomodulation in human myocardial disease.
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.
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Meij et al. (2002) studied Isoproterenol-induced myocardial injury. FGF-2 overexpression vs. Non-transgenic mice was evaluated on Myocardial damage score by histopathological evaluation. Overexpression of FGF-2 in transgenic mice exacerbated isoproterenol-induced myocardial damage, an effect that was dependent on T cell infiltration and reversed by T cell suppressors.
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