Inhibition of P38 MAPK Reduces Tumor Conditioned Medium-Induced Angiogenesis in Co-Cultured Human Umbilical Vein Endothelial Cells and Fibroblasts

2007 ◽  
Vol 71 (5) ◽  
pp. 1162-1169 ◽  
Author(s):  
Jun YE ◽  
Li YUAN
Keyword(s):  
Endothelial Cells ◽  
Conditioned Medium ◽  
P38 Mapk ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals e0060 Resistin impairs fibrinolytic activity in human umbilical vein endothelial cells via p38 MAPK pathway

Heart ◽  
2010 ◽  
Vol 96 (Suppl 3) ◽  
pp. A19-A19
Author(s):  
L. Yuguang ◽  
Z. Qin ◽  
L. Dan ◽  
Y. Haiyan ◽  
H. Jing ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
P38 Mapk ◽  
Fibrinolytic Activity ◽  
Mapk Pathway ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
P38 Mapk Pathway ◽  
Umbilical Vein Endothelial Cells

Abstract 43: A20 Plays as a Regulator in Tnfα-induced Injury of Human Umbilical Vein Endothelial Cells Through Tak1-dependent Pathway

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Lei Li ◽  
Jiafeng Lin ◽  
Maoping Chu ◽  
Kangting Ji ◽  
Lianpin Wu
Keyword(s):  
Endothelial Cells ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Umbilical Vein ◽  
No Production ◽  
Enos Expression ◽  
Mapk Phosphorylation ◽  
Human Umbilical Vein ◽  
Over Expression ◽  
Umbilical Vein Endothelial Cells

A20, a negative regulator of nuclear factor κB signaling, has been shown to attenuate atherosclerotic events. Transforming growth factor beta-activated kinase 1 (TAK1) plays a critical role in TNFα-induced atherosclerosis via endothelial nitric oxide (NO) synthase (eNOS) uncoupling and NO reduction. Aims: In the study, we investigated the hypothesis that A20 protected endothelial cells induced by TNFα through modulating eNOS activity and TAK1 signalling. Human umbilical vein endothelial cells (HUVECs) were stimulated by TNFα. The impact of A20 on cell apoptosis, eNOS expression and NO production and related TAK1 pathway were detected. Both eNOS and NO production were remarkably reduced, TAK1and p38 MAPK phosphorylation, HUVECs apoptosis increased after TNFα stimulation for 2 hrs, all of which were effectively attenuated by A20 over-expression. Inhibition of A20 significantly activated TAK1, p38 MAPK phosphorylation, and cell apoptosis, but eNOS expression, NO production decreased. Furthermore, p38 MAPK expression was suppressed by A20 over-expression, but re-enhanced by inhibiting A20 or activation of TAK1. Furtherly, TNFα-induced suppression of eNOS and NO production were largely prevented by silencing p38 MAPK. Collectively, our results suggested that A20-mediated TAK1 inactivation suppresses p38 MAPK and regulated MAPK/eNOS pathway, which contributes to endothelial cell survival and function preservation.

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