Fibroblast growth factor-1 improves cardiac functional recovery and enhances cell survival after ischemia and reperfusion: a fibroblast growth factor receptor, protein kinase C, and tyrosine kinase-dependent mechanism.

Abstract

OBJECTIVES:

We sought to investigate the role of fibroblast growth factor (FGF)-1 during acute myocardial ischemia and reperfusion.

BACKGROUND:

The FGFs display cardioprotective effects during ischemia and reperfusion.

METHODS:

We investigated FGF-1-induced cardioprotection during ischemia and reperfusion and the intracellular signaling pathways responsible for these effects in an ex vivo murine setup of myocardial ischemia and reperfusion.

RESULTS:

Cardiac-specific human FGF-1 overexpression was associated with enhanced post-ischemic hemodynamic recovery and decreased lactate dehydrogenase release during reperfusion. Inhibition of the FGF receptor, protein kinase C (PKC), and tyrosine kinase (TK) resulted in blockade of FGF-1-induced protective effects on cardiac functional recovery and cell death.

CONCLUSIONS:

The overexpression of FGF-1 induces cardioprotection through a pathway that involves the FGF receptor, PKC, and TK.

• Authors: Meindert Palmen, Mat J A P Daemen, Leon J De Windt, Jodil Willems, Willem R M Dassen, Sylvia Heeneman, Rene Zimmermann, Marc Van Bilsen, Pieter A Doevendans
• Journal: Journal of the American College of Cardiology (J Am Coll Cardiol) Vol. 44 Issue 5 Pg. 1113-23 (Sep 01 2004) ISSN: 1558-3597 [Electronic] United States
• PMID: 15337227 (Publication Type: Journal Article)

Chemical References

• Pyrroles
• Receptors, Fibroblast Growth Factor
• SU 5402
• Fibroblast Growth Factor 1
• Protein-Tyrosine Kinases
• Protein Kinase C

Topics

• Animals
• Blotting, Western
• Cell Survival (physiology)
• Fibroblast Growth Factor 1 (metabolism, physiology)
• Heart Ventricles (metabolism)
• Hemodynamics
• Immunohistochemistry
• In Vitro Techniques
• Male
• Mice
• Mice, Transgenic
• Myocardial Ischemia (physiopathology)
• Myocardial Reperfusion
• Precipitin Tests
• Protein Kinase C (physiology)
• Protein-Tyrosine Kinases (antagonists & inhibitors, physiology)
• Pyrroles (pharmacology)
• Receptors, Fibroblast Growth Factor (physiology)
• Recovery of Function (physiology)
• Signal Transduction (physiology)