scholarly journals Placenta Growth Factor-induced Early Growth Response 1 (Egr-1) Regulates Hypoxia-inducible Factor-1α (HIF-1α) in Endothelial Cells

2010 ◽  
Vol 285 (27) ◽  
pp. 20570-20579 ◽  
Author(s):  
Nitin Patel ◽  
Vijay K. Kalra
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Growth Response ◽  
Hypoxia Inducible Factor ◽  
Early Growth ◽  
Placenta Growth Factor ◽  
Early Growth Response ◽  
Hypoxia Inducible Factor 1Α ◽  
Early Growth Response 1

scholarly journals Increased Expression of the Transforming Growth Factor-β Signaling Pathway, Endoglin, and Early Growth Response-1 in Stable Plaques

Stroke ◽  
2009 ◽  
Vol 40 (2) ◽  
pp. 439-447 ◽  
Author(s):  
Pieter T.G. Bot ◽  
Imo E. Hoefer ◽  
Joost P.G. Sluijter ◽  
Patrick van Vliet ◽  
Anke M. Smits ◽  
...  
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Growth Response ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Early Growth ◽  
Early Growth Response ◽  
Early Growth Response 1

scholarly journals Smad-Independent Transforming Growth Factor-β Regulation of Early Growth Response-1 and Sustained Expression in Fibrosis

2008 ◽  
Vol 173 (4) ◽  
pp. 1085-1099 ◽  
Author(s):  
Swati Bhattacharyya ◽  
Shu-Jen Chen ◽  
Minghua Wu ◽  
Matthew Warner-Blankenship ◽  
Hongyan Ning ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Response ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Early Growth ◽  
Early Growth Response ◽  
Early Growth Response 1

scholarly journals Serine 26 in Early Growth Response‐1 Is Critical for Endothelial Proliferation, Migration, and Network Formation

2021 ◽  
Author(s):  
Fernando S. Santiago ◽  
Yue Li ◽  
Levon M. Khachigian
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Response ◽  
Network Formation ◽  
Early Growth ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Early Growth Response ◽  
Early Growth Response 1

Background Vascular endothelial cell proliferation, migration, and network formation are key proangiogenic processes involving the prototypic immediate early gene product, Egr‐1 (early growth response‐1). Egr‐1 undergoes phosphorylation at a conserved Ser26 but its function is completely unknown in endothelial cells or any other cell type. Methods and Results A CRISPR/Cas9 strategy was used to introduce a homozygous Ser26>Ala mutation into endogenous Egr‐1 in human microvascular endothelial cells. In the course of generating mutant cells, we produced cells with homozygous deletion in Egr ‐1 caused by frameshift and premature termination. We found that Ser26 mutation in Egr‐1, or Egr‐1 deletion, perturbed endothelial cell proliferation in models of cell counting or real‐time growth using the xCELLigence System. We found that Ser26 mutation or Egr‐1 deletion ameliorated endothelial cell migration toward VEGF‐A 165 (vascular endothelial growth factor‐A) in a dual‐chamber model. On solubilized basement membrane preparations, Ser26 mutation or Egr‐1 deletion prevented endothelial network (or tubule) formation, an in vitro model of angiogenesis. Flow cytometry further revealed that Ser26 mutation or Egr‐1 deletion elevated early and late apoptosis. Finally, we demonstrated that Ser26 mutation or Egr‐1 deletion increased VE‐cadherin (vascular endothelial cadherin) expression, a regulator of endothelial adhesion and signaling, permeability, and angiogenesis. Conclusions These findings not only indicate that Egr‐1 is essential for endothelial cell proliferation, migration, and network formation, but also show that point mutation in Ser26 is sufficient to impair each of these processes and trigger apoptosis as effectively as the absence of Egr‐1. This highlights the importance of Ser26 in Egr‐1 for a range of proangiogenic processes.

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