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Am J Physiol Heart Circ Physiol 280: H1039-H1050, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 3, H1039-H1050, March 2001

Overexpression of FGF-2 increases cardiac myocyte viability after injury in isolated mouse hearts

Farah Sheikh1, David P. Sontag1, Robert R. Fandrich2, Elissavet Kardami2, and Peter A. Cattini1

1 Department of Physiology, University of Manitoba, Winnipeg, Manitoba, R3E 3J7; and 2 Department of Human Anatomy and Cell Science, Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada R2H 2A6

We generated transgenic (TG) mice overexpressing fibroblast growth factor (FGF)-2 protein (22- to 34-fold) in the heart. Chronic FGF-2 overexpression revealed no significant effect on heart weight-to-body weight ratio or expression of cardiac differentiation markers. There was, however, a significant 20% increase in capillary density. Although there was no change in FGF receptor-1 expression, relative levels of phosphorylated c-Jun NH2-terminal kinase and p38 kinase as well as of membrane-associated protein kinase C (PKC)-alpha and total PKC-epsilon were increased in FGF-2-TG mouse hearts. An isolated mouse heart model of ischemia-reperfusion injury was used to assess the potential of increased endogenous FGF-2 for cardioprotection. A significant 34-45% increase in myocyte viability, reflected in a decrease in lactate dehydrogenase released into the perfusate, was observed in FGF-2 overexpressing mice and non-TG mice treated exogenously with FGF-2. In conclusion, FGF-2 overexpression causes augmentation of signal transduction pathways and increased resistance to ischemic injury. Thus, stimulation of endogenous FGF-2 expression offers a potential mechanism to enhance cardioprotection.

fibroblast growth factor; transgenic mice; cardioprotection; Langendorff preparation


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