scholarly journals Arterial-venous endothelial cell fate is related to vascular endothelial growth factor and Notch status during human bone mesenchymal stem cell differentiation

FEBS Letters ◽  
2008 ◽  
Vol 582 (19) ◽  
pp. 2957-2964 ◽  
Author(s):  
Gang Zhang ◽  
Jianye Zhou ◽  
Quanxin Fan ◽  
Zhe Zheng ◽  
Fusheng Zhang ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Stem Cell ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Mesenchymal Stem Cell ◽  
Cell Fate ◽  
Stem Cell Differentiation ◽  
Vascular Endothelial ◽  
Mesenchymal Stem Cell Differentiation ◽  
Endothelial Growth Factor

scholarly journals An exquisite cross-control mechanism among endothelial cell fate regulators directs the plasticity and heterogeneity of lymphatic endothelial cells

Blood ◽  
2010 ◽  
Vol 116 (1) ◽  
pp. 140-150 ◽  
Author(s):  
Jinjoo Kang ◽  
Jaehyuk Yoo ◽  
Sunju Lee ◽  
Wanli Tang ◽  
Berenice Aguilar ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Fate ◽  
Control Mechanism ◽  
Lymphatic Endothelial Cell ◽  
Notch Receptor ◽  
Vascular Endothelial ◽  
Cell Fates ◽  
Endothelial Growth Factor

Abstract Arteriovenous-lymphatic endothelial cell fates are specified by the master regulators, namely, Notch, COUP-TFII, and Prox1. Whereas Notch is expressed in the arteries and COUP-TFII in the veins, the lymphatics express all 3 cell fate regulators. Previous studies show that lymphatic endothelial cell (LEC) fate is highly plastic and reversible, raising a new concept that all 3 endothelial cell fates may coreside in LECs and a subtle alteration can result in a reprogramming of LEC fate. We provide a molecular basis verifying this concept by identifying a cross-control mechanism among these cell fate regulators. We found that Notch signal down-regulates Prox1 and COUP-TFII through Hey1 and Hey2 and that activated Notch receptor suppresses the lymphatic phenotypes and induces the arterial cell fate. On the contrary, Prox1 and COUP-TFII attenuate vascular endothelial growth factor signaling, known to induce Notch, by repressing vascular endothelial growth factor receptor-2 and neuropilin-1. We show that previously reported podoplanin-based LEC heterogeneity is associated with differential expression of Notch1 in human cutaneous lymphatics. We propose that the expression of the 3 cell fate regulators is controlled by an exquisite feedback mechanism working in LECs and that LEC fate is a consequence of the Prox1-directed lymphatic equilibrium among the cell fate regulators.

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