Propranolol induces apoptosis of human umbilical vein endothelial cells through down-regulation of CD147

2012 ◽  
pp. no-no ◽  
Author(s):  
W. Xie ◽  
H. Xie ◽  
F. Liu ◽  
W. Li ◽  
J. Dan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Down Regulation ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Lysophosphatidylcholine Decreases the Synthesis of Tissue Factor Pathway Inhibitor in Human Umbilical Vein Endothelial Cells

1998 ◽  
Vol 79 (01) ◽  
pp. 217-221 ◽  
Author(s):  
Koichi Kokame ◽  
Toshiyuki Miyata ◽  
Naoaki Sato ◽  
Hisao Kato
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Umbilical Vein ◽  
Mrna Levels ◽  
Down Regulation ◽  
Human Umbilical Vein ◽  
Tissue Factor Pathway ◽  
Umbilical Vein Endothelial Cells

SummaryThrombotic complications are frequently associated with atherosclerosis. Lysophosphatidylcholine (LPC), a component accumulated in oxidatively modified LDL (ox-LDL), is known to play a crucial role in the initiation and progression of atherosclerotic vascular lesions. Since a vascular anticoagulant, tissue factor pathway inhibitor (TFPI), has the function of regulating the initial reaction of tissue factor (TF)-induced coagulation, we investigated the effect of LPC on TFPI synthesis in cultured human umbilical vein endothelial cells (HUVEC). The treatment of HUVEC with LPC for 24 h decreased TFPI antigen levels in both the culture medium and the cell lysate in a dose-dependent manner. Northern blot analysis revealed that LPC caused a time-dependent decrease in the TFPI mRNA levels. The levels of TFPI antigen and mRNA were decreased to 72% and 38%, respectively, by the incubation with 50 μM LPC for 24 h. The down-regulation by LPC of TFPI mRNA expression was not observed in the presence of cycloheximide, suggesting that protein synthesis was involved in the suppression of TFPI mRNA expression. The TFPI mRNA levels in actinomycin D-treated cells were relatively stable, indicating that the down-regulation of TFPI mRNA by LPC would be partly explained by the enhanced mRNA destabilization. In contrast to the significant down-regulatory effects of LPC on TFPI expression, LPC did not induce TF mRNA expression in HUVEC. These results indicate that LPC accumulated in the atherosclerotic vascular wall would suppress endothelial TFPI synthesis, reducing the antithrombotic property of endothelial cells.

scholarly journals Down-Regulation of MicroRNA-137 Improves High Glucose-Induced Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells by Up-Regulation of AMPKα1

2016 ◽  
Vol 39 (3) ◽  
pp. 847-859 ◽  
Author(s):  
Jie Li ◽  
Junfeng Li ◽  
Tingting Wei ◽  
Junhua Li
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Protective Effect ◽  
Cell Viability ◽  
Vascular Injury ◽  
High Glucose ◽  
Umbilical Vein ◽  
Down Regulation ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Background/Aims: To investigate the effects of miR-137 on high glucose (HG)-induced vascular injury, and to establish the mechanism underlying these effects. Methods: Human umbilical vein endothelial cells (HUVECs) were transfected with miR-137 inhibitor or mimic, and then treated with normal or high glucose. Cell viability and apoptosis were detected by using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. Reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) were detected by fluorescent probe (DCFH-DA), thiobarbituric acid reaction, and the nitroblue tetrazolium assay, respectively. The mRNA and protein expressions of AMPKα1 were determined by qRT-PCR and Western blotting. Results: Down-regulation of miR-137 dramatically reverted HG-induced decreases in cell viability and SOD levels and increases in apoptosis, ROS and MDA levels. Moreover, bioinformatics analysis predicted that the AMPKα1 was a potential target gene of miR-137. Luciferase reporter assay demonstrated that miR-137 could directly target AMPKα1. AMPKα1 overexpression had the similar effect as miR-137 inhibition. Down-regulation of AMPKα1 in HUVECs transfected with miR-137 inhibitor partially reversed the protective effect of miR-137 inhibition on HG-induced oxidative stress in HUVECs. Conclusion: Down-regulation of miR-137 ameliorates HG-induced injury in HUVECs by overexpression of AMPKα1, leading to increasing cellular reductive reactions and decreasing oxidative stress. These results provide further evidence for protective effect of miR-137 inhibition on HG-induced vascular injury.

scholarly journals Reversible Protease-Activated Receptor 1 Downregulation Mediated by Ankaferd Blood Stopper Inducible With Lipopolysaccharides Inside the Human Umbilical Vein Endothelial Cells

2011 ◽  
Vol 17 (6) ◽  
pp. E165-E170 ◽  
Author(s):  
Afife Karabıyık ◽  
Sükrü Güleç ◽  
Erkan Yilmaz ◽  
Ibrahim Haznedaroglu ◽  
Nejat Akar
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Biological Response ◽  
Hemostatic Agent ◽  
Down Regulation ◽  
Human Umbilical Vein ◽  
Lps Challenge ◽  
Ankaferd Blood Stopper ◽  
Protease Activated Receptor 1 ◽  
Umbilical Vein Endothelial Cells

Ankaferd Blood Stopper (ABS) is a novel topical hemostatic agent with pleiotropic actions indicated in clinical hemorrhages. Protease-activated receptor 1 (PAR-1) is located in the crossroads of hemostasis, inflammation, infection, apoptosis and tumorigenesis. ABS-induced formation of the protein network with vital erythroid aggregation covers the entire physiological hemostatic process. The aim of this study is to assess the effects of ABS on PAR-1 in the Human Umbilical Vein Endothelial Cells (HUVEC) model, in relation to the “ipopolysaccharides (LPS)-challenge” to endothelium. For this purpose, ABS 10 μL and 100 μL, had been applied to HUVEC within the time periods of 5 minutes (min), 25 min, 50 min, 6 hours (h) and 24 h. The cells have lifted from the plastic surface and adhered to each other during theABSapplication to the HUVECs. After 24 hours the cells returned to normal baseline level. We observed dose-dependent reversible PAR-1 down-regulation mediated by ABS inside the human umbilical vein endothelial cells. ABS-induced sustained PAR-1 down-regulation in the presence of LPS. Those findings indicated that ABS hemostatic agent may act as a topical biological response modifier by acting on PAR-1 at the vascular endothelial and cellular level.

scholarly journals Thioredoxin reductase is the major selenoprotein expressed in human umbilical-vein endothelial cells and is regulated by protein kinase C

1999 ◽  
Vol 342 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Sue M. ANEMA ◽  
Simon W. WALKER ◽  
A. Forbes HOWIE ◽  
John R. ARTHUR ◽  
Fergus NICOL ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Umbilical Vein ◽  
Thioredoxin Reductase ◽  
Maximal Effect ◽  
Down Regulation ◽  
Human Umbilical Vein ◽  
Kinase C ◽  
Umbilical Vein Endothelial Cells

Damage to the endothelium by reactive oxygen species favours atherogenesis. Such damage can be prevented by selenium, which is thought to exert its actions through the expression of selenoproteins. The family of glutathione peroxidases (GPXs) may have antioxidant roles in the endothelium but other intracellular and extracellular selenoproteins with antioxidant actions may also be important. The selenoproteins expressed by cultured human umbilical-vein endothelial cells (HUVECs) were labelled with [75Se]selenite and separated using SDS/PAGE. HUVECs secreted no extracellular selenoproteins. There were distinct differences between the intracellular selenoprotein profile of 75Se-labelled HUVECs and those of other tissues. A single selenoprotein with a molecular mass of 58 kDa accounted for approx. 43% of the intracellular 75Se-labelled proteins in HUVECs. This protein was identified by Western blotting as the redox-active lipid-hydroperoxide-detoxifying selenoprotein, thioredoxin reductase (TR). TR expression in HUVECs was down-regulated by transiently exposing cells to the phorbol ester PMA for periods as short as 1 min. However, there was a delay of 48 h after PMA exposure before maximal down-regulation of TR was observed. The protein kinase C (PKC) inhibitor bisindolylmaleimide I hydrochloride had no effect on TR expression when added alone, but the agent prevented the down-regulation of TR expression seen with PMA. The calcium ionophore A23187 increased TR expression in HUVECs after a 12-h exposure, but the maximal effect was only observed after a 35-h exposure. These findings suggest that TR may be an important factor in the known ability of Se to protect HUVECs from peroxidative damage. Furthermore, the results also suggest that TR expression can be negatively regulated through PKC. It is possible that TR expression may be positively regulated by the calcium-signalling cascade, although TR induction by A23187 may be due to toxicity.

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