scholarly journals Lentiviral Rescue of Vascular Endothelial Growth Factor Receptor-2 Expression inFlk1−/− Embryonic Stem Cells Shows Early Priming of Endothelial Precursors

Stem Cells ◽  
2007 ◽  
Vol 25 (12) ◽  
pp. 2987-2995 ◽  
Author(s):  
Xiujuan Li ◽  
Dan Edholm ◽  
Fredrik Lanner ◽  
Georg Breier ◽  
Filip Farnebo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Growth Factor ◽  
Embryonic Stem Cells ◽  
Growth Factor ◽  
Embryonic Stem ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Endothelial Precursors

scholarly journals A Novel Role for Vascular Endothelial Growth Factor as an Autocrine Survival Factor for Embryonic Stem Cells during Hypoxia

2004 ◽  
Vol 280 (5) ◽  
pp. 3493-3499 ◽  
Author(s):  
Koen Brusselmans ◽  
Françoise Bono ◽  
Désiré Collen ◽  
Jean-Marc Herbert ◽  
Peter Carmeliet ◽  
...  
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Growth Factor ◽  
Embryonic Stem Cells ◽  
Growth Factor ◽  
Embryonic Stem ◽  
Vascular Endothelial ◽  
Survival Factor ◽  
Endothelial Growth Factor

Vascular endothelial growth factor promotes cardiomyocyte differentiation of embryonic stem cells

2006 ◽  
Vol 291 (4) ◽  
pp. H1653-H1658 ◽  
Author(s):  
Yu Chen ◽  
Ivo Amende ◽  
Thomas G. Hampton ◽  
Yinke Yang ◽  
Qingen Ke ◽  
...  
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Growth Factor ◽  
Embryonic Stem Cells ◽  
Growth Factor ◽  
Troponin I ◽  
Embryonic Stem ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Cardiomyocyte Differentiation ◽  
Endothelial Growth Factor

Embryonic stem cells (ESCs) overexpressing the vascular endothelial growth factor (VEGF) improve cardiac function in mouse models of myocardial ischemia and infarction by mechanisms that are poorly understood. Here we studied the effects of VEGF on cardiomyocyte differentiation of mouse ESCs in vitro. We used flow cytometry to determine the expression of α-myosin heavy chain (α-MHC), cardiac troponin I (cTn-I), and Nkx2.5 in differentiated ESCs. VEGF (20 ng/ml) significantly enhanced α-MHC, cTn-I, and Nkx2.5 expression in differentiated ESCs. Western blot analysis confirmed these findings. We found that VEGF receptor FMS-like tyrosine kinase-1 (Flt-1) and fetal liver kinase-1 (Flk-1) expression increased during ESC differentiation. Antibodies against Flk-1 totally blocked and against Flt-1 partially blocked VEGF-induced NKx2.5-positive-stained cells. The ERK inhibitor PD-098059 abolished VEGF-induced cardiomyocyte differentiation of ESCs. Our results suggest that VEGF promotes cardiomyocyte differentiation predominantly by ERK-mediated Flk-1 activation and, to a lesser extent, by Flt-1 activation. These findings may be of significance for stem cell and growth factor therapies to regenerate failing cardiomyocytes.

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