Linolelaidic acid induces apoptosis, cell cycle arrest and inflammation stronger than elaidic acid in human umbilical vein endothelial cells through lipid rafts

2016 ◽  
Vol 119 (7) ◽  
pp. 1600374 ◽  
Author(s):  
Jing Li ◽  
Huan Rao ◽  
Qiu Bin ◽  
Ya-Wei Fan ◽  
Hong-Yan Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Cell Cycle Arrest ◽  
Lipid Rafts ◽  
Elaidic Acid ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Cycle Arrest ◽  
Umbilical Vein Endothelial Cells

scholarly journals Potential Pathways Involved in Elaidic Acid Induced Atherosclerosis in Human Umbilical Vein Endothelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-10
Author(s):  
Huahong Yu ◽  
Xiangmei Li ◽  
Zhongshang Liang ◽  
Bin Qiu ◽  
Siguang Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Elaidic Acid ◽  
Umbilical Vein ◽  
Underlying Mechanism ◽  
Pcr Analysis ◽  
Control Group ◽  
Apoptosis Pathway ◽  
Human Umbilical Vein ◽  
Cycle Arrest ◽  
Umbilical Vein Endothelial Cells

Researches have demonstrated that trans-fatty acids are related to the progression of atherosclerosis, but the underlying mechanism is not clear till now. In the presented study, two-dimensional electrophoresis based proteomics was used to discover the role of elaidic acid in atherosclerosis. In human umbilical vein endothelial cells (HUVEC), twenty-two and twenty-three differentially expressed proteins were identified in low (50 μmol/L) and high (400 μmol/L) concentration elaidic acid simulated groups, respectively, comparing with the control group. The expressions of some selected proteins (PSME3, XRCC5, GSTP1, and GSTO1) were validated by qRT-PCR analysis. Western blotting analysis further confirmed that elaidic acid downregulated the expression of PSME3 and XRCC5. Moreover, P53, the downstream protein of PSME3, was further investigated. Results demonstrated that a variety of proteins, many of which were related to oxidative stress, apoptosis, and DNA damage, were involved in the elaidic acid induced atherosclerosis. Furthermore, P53 was demonstrated to regulate the atherosclerosis through cell cycle arrest and apoptosis pathway.

Lipid Rafts Promote trans Fatty Acid-Induced Inflammation in Human Umbilical Vein Endothelial Cells

Lipids ◽  
2016 ◽  
Vol 52 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Yao Pan ◽  
Benxin Liu ◽  
Zeyuan Deng ◽  
Yawei Fan ◽  
Jing Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Fatty Acid ◽  
Lipid Rafts ◽  
Trans Fatty Acid ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Caspase pathway of elaidic acid (9t-C18:1)-induced apoptosis in human umbilical vein endothelial cells

2012 ◽  
Vol 36 (3) ◽  
pp. 255-260 ◽  
Author(s):  
Bin Qiu ◽  
Jiang‑Ning Hu ◽  
Rong Liu ◽  
Ya‑Wei Fan ◽  
Jing Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Elaidic Acid ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Caspase Pathway ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

Propranolol Suppresses Cobalt Chloride-Induced Hypoxic Proliferation in Human Umbilical Vein Endothelial Cells in vitro

Pharmacology ◽  
2018 ◽  
Vol 103 (1-2) ◽  
pp. 61-67 ◽  
Author(s):  
Li Wei ◽  
Li Li ◽  
Bin Zhang ◽  
Lin Ma
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Cyclin D1 ◽  
Cobalt Chloride ◽  
Umbilical Vein ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Background/Aims: To investigate the effect of propranolol on cobalt chloride (CoCl2)-induced hypoxic proliferation in human umbilical vein endothelial cells (HUVECs). Methods: CoCl2 was administrated to HUVECs to mimic hypoxic proliferation in infantile hemangioma. The proliferation of HUVECs was detected by Cell Counting Kit-8. Effects of propranolol on apoptosis and expressions of cell cycle-related genes, CDK4 and cyclin D1, were detected by flow cytometry and RT-PCR respectively. The release of vascular endothelial growth factor (VEGF) and lactate dehydrogenase (LDH) was measured by enzyme-linked immunosorbent assay. Results: Propranolol significantly inhibited the CoCl2-induced hypoxic proliferation of HUVECs in a dose-dependent manner, and also induced apoptosis and suppressed the expression of CDK4 and cyclin D1. Propranolol also decreased the release of VEGF and LDH in the supernatant. Conclusions: Propranolol could inhibit CoCl2-induced hypoxic proliferation of HUVECs through inducing apoptosis and cell cycle arrest.

Sign in / Sign up

Export Citation Format

Share Document