Enhancement on Primate Corneal Endothelial Cell Survival In Vitro by a ROCK Inhibitor

2009 ◽  
Vol 50 (8) ◽  
pp. 3680 ◽  
Author(s):  
Naoki Okumura ◽  
Morio Ueno ◽  
Noriko Koizumi ◽  
Yuji Sakamoto ◽  
Kana Hirata ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Survival ◽  
Corneal Endothelial Cell ◽  
Rock Inhibitor ◽  
Endothelial Cell Survival

scholarly journals Regulatory T cells promote corneal endothelial cell survival following transplantation via interleukin‐10

2019 ◽  
Vol 20 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Giulia Coco ◽  
William Foulsham ◽  
Takeshi Nakao ◽  
Jia Yin ◽  
Afsaneh Amouzegar ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cell ◽  
Regulatory T Cells ◽  
Cell Survival ◽  
Interleukin 10 ◽  
Corneal Endothelial Cell ◽  
Endothelial Cell Survival

The effects of various growth factors on endothelial cell survival in vitro

1989 ◽  
Vol 162 (3) ◽  
pp. 1010-1016 ◽  
Author(s):  
Takafumi Etoh ◽  
Kazuhiko Takehara ◽  
Atsuyuki Igarashi ◽  
Yasumasa Ishibashi
Keyword(s):  
Growth Factors ◽  
Endothelial Cell ◽  
Cell Survival ◽  
Endothelial Cell Survival

Signaling and regulation of endothelial cell survival by angiopoietin-2

2006 ◽  
Vol 291 (4) ◽  
pp. H1635-H1645 ◽  
Author(s):  
Rania Harfouche ◽  
Sabah N. A. Hussain
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Cell Survival ◽  
Umbilical Vein ◽  
Biological Effects ◽  
Pi3 Kinase ◽  
Endothelial Cell Migration ◽  
Endothelial Cell Survival ◽  
Induced Apoptosis

Angiopoietins are ligands for endothelial cell-specific Tie-2 receptors. Whereas angiopoietin-1 (Ang-1) activates these receptors and promotes cell survival, migration, and sprouting, little information is available regarding how Ang-2 influences these cells. In this study, we evaluated signaling pathways and biological effects of physiological concentrations of Ang-2 in cultured human umbilical vein endothelial cells. Ang-2 at 150 and 300 ng/ml elicited a transient (reaching peak values within 15 min of exposure) increase in the phosphorylation of Tie-2 receptors, protein kinase B (Akt), ERK1/2, and p38 members of the mitogen-activated protein kinases. However, unlike Ang-1, Ang-2 significantly inhibited JNK/SAPK phosphorylation. When vascular endothelial growth factor (VEGF) was present along with Ang-2, ERK1/2 phosphorylation was inhibited, whereas augmentation of Ang-1-induced ERK1/2 phosphorylation was triggered by VEGF. Ang-2 treatment had no effect on cell migration and in vitro wound healing but significantly attenuated serum deprivation-induced apoptosis and promoted survival. These effects were completely reversed by phosphatidylinositol 3 (PI3)-kinase and ERK1/2 inhibitors but were augmented by an inhibitor of the p38 pathway. These results suggest that Ang-2 promotes endothelial cell survival through the ERK1/2 and PI3-kinase pathways and that this angiopoietin is not a strong promoter of endothelial cell migration. We also conclude that the nature of interactions in terms of ERK1/2 activation between Ang-2 and VEGF is different from that of Ang-1 and VEGF.

The effects of scleroderma sera on endothelial cell survival in vitro

1990 ◽  
Vol 282 (8) ◽  
pp. 516-519 ◽  
Author(s):  
T. Etoh ◽  
A. Igarashi ◽  
K. Iozumi ◽  
Y. Ishibashi ◽  
K. Takehara
Keyword(s):  
Endothelial Cell ◽  
Cell Survival ◽  
Endothelial Cell Survival
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