The role of tyrosine phosphorylation in TNFα-induced apoptosis of Human Umbilical Vein Endothelial Cells (HUVECs)

2001 ◽  
Vol 29 (5) ◽  
pp. A113-A113
Author(s):  
Y. M. O'Dowd ◽  
S.H. Teh ◽  
A.D.K. Hill ◽  
E. McDermott ◽  
N. O'Higgins
2009 ◽  
Vol 204 (2) ◽  
pp. 353-358 ◽  
Author(s):  
Bimei Jiang ◽  
Pengfei Liang ◽  
Bing Zhang ◽  
Juan Song ◽  
Xiaoyuan Huang ◽  
...  

2019 ◽  
Vol 316 (5) ◽  
pp. H1178-H1191 ◽  
Author(s):  
Ling Yang ◽  
Yujie Zhang ◽  
Yadong Ma ◽  
Jun Du ◽  
Luo Gu ◽  
...  

Melatonin is a natural hormone involved in the regulation of circadian rhythm, immunity, and cardiovascular function. In the present study, we focused on the mechanism of melatonin in the regulation of vascular permeability. We found that melatonin could inhibit both VEGF- and EGF-induced monolayer permeability of human umbilical vein endothelial cells (HUVECs) and change the tyrosine phosphorylation of vascular-endothelial (VE-)cadherin, which was related to endothelial barrier function. In addition, phospho-AKT (Ser473) and phospho-ERK(1/2) played significant roles in the regulation of VE-cadherin phosphorylation. Both the phosphatidylinositol 3-kinase/AKT inhibitor LY49002 and MEK/ERK inhibitor U0126 could inhibit the permeability of HUVECs, but with different effects on tyrosine phosphorylation of VE-cadherin. Melatonin can influence the two growth factor-induced phosphorylation of AKT (Ser473) but not ERK(1/2). Our results show that melatonin can inhibit growth factor-induced monolayer permeability of HUVECs by influencing the phosphorylation of AKT and VE-cadherin. Melatonin can be a potential treatment for diseases associated with abnormal vascular permeability. NEW & NOTEWORTHY We found that melatonin could inhibit both EGF- and VEGF-induced monolayer permeability of human umbilical vein endothelial cells, which is related to phosphorylation of vascular-endothelial cadherin. Blockade of phosphatidylinositol 3-kinase/AKT and MEK/ERK pathways could inhibit the permeability of human umbilical vein endothelial cells, and phosphorylation of AKT (Ser473) might be a critical event in the changing of monolayer permeability and likely has cross-talk with the MEK/ERK pathway.


2016 ◽  
Vol 117 (07) ◽  
pp. 376-380 ◽  
Author(s):  
K. Kamali ◽  
E. Salmani Korjan ◽  
E. Eftekhar ◽  
K. Malekzadeh ◽  
F. Ghadiri Soufi

Sign in / Sign up

Export Citation Format

Share Document