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Cardiovascular Research 2002 55(4):768-777; doi:10.1016/S0008-6363(02)00494-7
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Angiogenesis-independent cardioprotection in FGF-1 transgenic mice

Alexandra Buehlera, Alessandra Martirea,1, Claudia Strohma,1, Swen Wolframa, Borja Fernandeza, Meindert Palmenb, Xander H.T Wehrensb, Pieter A Doevendansb, Wolfgang M Franzd, Wolfgang Schapera and René Zimmermannc,*

aDepartment of Experimental Cardiology, Max-Planck-Institute, D-61231 Bad Nauheim, Germany
bCardiovascular Research Institute Maastricht, 6202 AZ Maastricht, The Netherlands
cDepartment of Vascular Genomics, Kerckhoff Clinic, Benekestr. 2–8, D-61231 Bad Nauheim, Germany
dMedizinische Universitätsklinik, D-23538 Lübeck, Germany

* Corresponding author. Tel.: +49-6032-996-2801; fax: +49-6032-996-2809 r.zimmer{at}vascular-genomics.de

Objective: This study was performed to evaluate the cardioprotective role of acidic fibroblast growth factor-1 (FGF-1) in transgenic mice with cardiac-specific overexpression of human FGF-1. Methods: Mice were subjected to coronary artery occlusion for 15–75 min with a continuously recorded 3-lead electrocardiogram (ECG). Infarct size was measured and ERK-1 and -2 activity was assessed by Western blot analysis. Creatine kinase and lactate dehydrogenase activity as marker for cell viability were measured in isolated ventricular myocytes subjected to simulated ischemia. Results: Infarct development was markedly delayed in transgenics with first signs of myocardial infarction visible at 45 min after coronary artery occlusion compared to 15 min in wildtype. Maximal infarct size (60% of risk area) did not differ, but transgenics reached maximal infarction after 75 min compared to 45 min in wildtype animals. ECG revealed delayed Q-wave development and delayed ST-segment elevation in transgenics. Creatine kinase and lactate dehydrogenase release was significantly attenuated from isolated transgenic myocytes at 4 and 8 h after simulated ischemia. The delay in infarct development is partially due to a constitutive higher expression of the extracellular signal-regulated kinases ERK-1 and -2 in the myocardium of transgenics. Additionally, injection of the ERK-1/2 inhibitor UO126 decreased the cardioprotective effect of FGF-1. Conclusion: Cardiac specific overexpression of FGF-1 provides cardioprotection at the level of the cardiac myocyte, independent from angiogenesis, and at least partially mediated via activation of the mitogen activated protein kinase (MAP) ERK-1 and -2.

KEYWORDS Ventricular function; Hemodynamics; Signal transduction; Ischemia; ECG

1 Both authors contributed equally to this study.


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