scholarly journals Fibroblast growth factor 2 is an essential cardioprotective factor in a closed-chest model of cardiac ischemia-reperfusion injury

2015 ◽  
Vol 3 (1) ◽  
pp. e12278 ◽  
Author(s):  
Stacey L. House ◽  
Joy Wang ◽  
Angela M. Castro ◽  
Carla Weinheimer ◽  
Attila Kovacs ◽  
...  
Keyword(s):  
Growth Factor ◽  
Reperfusion Injury ◽  
Fibroblast Growth Factor ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Closed Chest

scholarly journals Endothelial fibroblast growth factor receptor signaling is required for vascular remodeling following cardiac ischemia-reperfusion injury

2016 ◽  
Vol 310 (5) ◽  
pp. H559-H571 ◽  
Author(s):  
Stacey L. House ◽  
Angela M. Castro ◽  
Traian S. Lupu ◽  
Carla Weinheimer ◽  
Craig Smith ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Reperfusion Injury ◽  
Fibroblast Growth Factor ◽  
Vascular Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Fibroblast Growth ◽  
Hypertrophic Response

Fibroblast growth factor (FGF) signaling is cardioprotective in various models of myocardial infarction. FGF receptors (FGFRs) are expressed in multiple cell types in the adult heart, but the cell type-specific FGFR signaling that mediates different cardioprotective endpoints is not known. To determine the requirement for FGFR signaling in endothelium in cardiac ischemia-reperfusion injury, we conditionally inactivated the Fgfr1 and Fgfr2 genes in endothelial cells with Tie2-Cre ( Tie2-Cre, Fgfr1f/f, Fgfr2f/fDCKO mice). Tie2-Cre, Fgfr1f/f, Fgfr2f/fDCKO mice had normal baseline cardiac morphometry, function, and vessel density. When subjected to closed-chest, regional cardiac ischemia-reperfusion injury, Tie2-Cre, Fgfr1f/f, Fgfr2f/fDCKO mice showed a significantly increased hypokinetic area at 7 days, but not 1 day, after reperfusion. Tie2-Cre, Fgfr1f/f, Fgfr2f/fDCKO mice also showed significantly worsened cardiac function compared with controls at 7 days but not 1 day after reperfusion. Pathophysiological analysis showed significantly decreased vessel density, increased endothelial cell apoptosis, and worsened tissue hypoxia in the peri-infarct area at 7 days following reperfusion. Notably, Tie2-Cre, Fgfr1f/f, Fgfr2f/fDCKO mice showed no impairment in the cardiac hypertrophic response. These data demonstrate an essential role for FGFR1 and FGFR2 in endothelial cells for cardiac functional recovery and vascular remodeling following in vivo cardiac ischemia-reperfusion injury, without affecting the cardiac hypertrophic response. This study suggests the potential for therapeutic benefit from activation of endothelial FGFR pathways following ischemic injury to the heart.

Intravenous Fibroblast Growth Factor Penetrates the Blood-Brain Barrier and Protects Hippocampal Neurons Against Ischemia-Reperfusion Injury

1998 ◽  
Vol 49 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Pedro Cuevas M.D., Ph.D., F.A.C.A. ◽  
Fernando Carceller M.D., Ph.D. ◽  
Isabel Muñoz-Willery B.Sc., Ph.D. ◽  
Guillermo Giménez-Gallego B.Sc., Ph.D.
Keyword(s):  
Growth Factor ◽  
Reperfusion Injury ◽  
Fibroblast Growth Factor ◽  
Blood Brain Barrier ◽  
Hippocampal Neurons ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Brain Barrier ◽  
Fibroblast Growth ◽  
Blood Brain
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