scholarly journals Leonurus sibiricusHerb Extract Suppresses Oxidative Stress and Ameliorates Hypercholesterolemia in C57BL/6 Mice and TNF-α Induced Expression of Adhesion Molecules and Lectin-Like Oxidized LDL Receptor-1 in Human Umbilical Vein Endothelial Cells

2010 ◽  
Vol 74 (2) ◽  
pp. 279-284 ◽  
Author(s):  
Min-Ja LEE ◽  
Hye-Sook LEE ◽  
Sun-Dong PARK ◽  
Hyung-In MOON ◽  
Won-Hwan PARK
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Umbilical Vein ◽  
Oxidized Ldl ◽  
Ldl Receptor ◽  
Induced Expression ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

scholarly journals VGLL4 Protects against Oxidized-LDL-Induced Endothelial Cell Dysfunction and Inflammation by Activating Hippo-YAP/TEAD1 Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Kaicheng Xu ◽  
Haomin Zhao ◽  
Xiaolei Qiu ◽  
Xiwen Liu ◽  
Fucheng Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Oxidized Ldl ◽  
Endothelial Cell Dysfunction ◽  
Human Umbilical Vein ◽  
Cell Dysfunction ◽  
Umbilical Vein Endothelial Cells

Vestigial-like 4 (VGLL4) has been found to have multiple functions in tumor development; however, its role in cardiovascular disease is unknown. The aim of this study was to investigate the effect of VGLL4 on the dysfunction and inflammatory response of Ox-LDL-induced human umbilical vein endothelial cells (HUVECs) and its mechanism, so as to provide a new theoretical basis for the diagnosis and treatment of atherosclerosis. In the present study, the protective activity of VGLL4 inhibiting Ox-LDL-induced apoptosis, oxidative stress, inflammation, and injury as well as its molecular mechanisms was examined using human umbilical vein endothelial cells (HUVECs). The results showed that the expression of VGLL4 was decreased with the increase of Ox-LDL concentration in HUVECs. In addition, the functional study found that VGLL4 overexpression alleviated Ox-LDL-induced oxidative stress, inflammation, and dysfunction and inhibited apoptosis. Further research found that VGLL4 regulated Hippo-YAP/TEAD1 signaling pathway, and the Hippo-YAP/TEAD1 signaling pathway was involved in the protective mechanism of VGLL4 on HUVECs. In conclusion, it suggests that VGLL4 protects against oxidized-LDL-induced endothelial cell dysfunction by activating the Hippo-YAP/TEAD1 signaling pathway.

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