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Am J Physiol Heart Circ Physiol 282: H1071-H1080, 2002. First published November 15, 2001; doi:10.1152/ajpheart.00290.2001
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Vol. 282, Issue 3, H1071-H1080, March 2002

Acute protection of ischemic heart by FGF-2: involvement of FGF-2 receptors and protein kinase C

Zhi-Sheng Jiang*, Raymond R. Padua*, Haisong Ju, Bradley W. Doble, Yan Jin, Jianming Hao, Peter A. Cattini, Ian M. C. Dixon, and Elissavet Kardami

Departments of Human Anatomy and Cell Sciences and Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada R2H 2A6

We examined the effect of fibroblast growth factor (FGF)-2 on myocardial resistance to injury when administered after the onset of ischemia, in vivo and ex vivo, and the role of FGF-2 receptors and protein kinase C (PKC). FGF-2 was injected into the left ventricle of rats undergoing permanent surgical coronary occlusion leading to myocardial infarction (MI). After 24 h, FGF-2-treated hearts displayed significantly reduced injury, determined by histological staining and troponin T release, and improved developed pressure compared with untreated controls. An FGF-2 mutant with diminished affinity for the tyrosine kinase FGF-2 receptor 1 (FGFR1) was not cardioprotective. FGF-2-treated hearts retained improved function and decreased damage at 6 wk after MI. In the ex vivo heart, FGF-2 administration during reperfusion after 30-min ischemia improved functional recovery and increased relative levels of PKC subtypes alpha , epsilon , and zeta  in the particulate fraction, in a chelerythrine-preventable mode; it also decreased loss of energy metabolites. We conclude that intramyocardial FGF-2 administration shortly after the onset of ischemia confers protection from acute and chronic cardiac dysfunction and damage; FGF-2 delivered during reperfusion protects from ischemia-reperfusion injury; and protection by FGF-2 requires intact binding to FGFR1 and is likely mediated by PKC.

cardioprotection; growth factors; reperfusion injury; signal transduction; protein therapy

* Z.-S. Jiang and R. R. Padua contributed equally to this work.




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