title: 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: OBJECTIVE
  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.affiliation: Department of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), The Netherlands.
authors.forename: Meindert
authors.initials: M
authors.lastname: Palmen
authors.forename: Mat J A P
authors.initials: MJ
authors.lastname: Daemen
authors.forename: Leon J
authors.initials: LJ
authors.lastname: De Windt
authors.forename: Jodil
authors.initials: J
authors.lastname: Willems
authors.forename: Willem R M
authors.initials: WR
authors.lastname: Dassen
authors.forename: Sylvia
authors.initials: S
authors.lastname: Heeneman
authors.forename: Rene
authors.initials: R
authors.lastname: Zimmermann
authors.forename: Marc
authors.initials: M
authors.lastname: Van Bilsen
authors.forename: Pieter A
authors.initials: PA
authors.lastname: Doevendans
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002470:Cell Survival / Q000502:physiology*; D016220:Fibroblast Growth Factor 1 / Q000378:metabolism / Q000502:physiology*; D006352:Heart Ventricles / Q000378:metabolism; D006439:Hemodynamics; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D011233:Precipitin Tests; D011493:Protein Kinase C / Q000502:physiology; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000502:physiology; D011758:Pyrroles / Q000494:pharmacology; D017468:Receptors, Fibroblast Growth Factor / Q000502:physiology; D020127:Recovery of Function / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
chemical_list: D011758:Pyrroles; D017468:Receptors, Fibroblast Growth Factor; C105686:SU 5402; D016220:Fibroblast Growth Factor 1; D011505:Protein-Tyrosine Kinases; D011493:Protein Kinase C