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.

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

scholarly journals The expression of Drosha, DGCR8, Dicer and Ago-2 genes are upregulated in human umbilical vein endothelial cells under hyperglycemic condition

2018 ◽  
Vol 52 (3) ◽  
pp. 123-127 ◽  
Author(s):  
Farhad Ghadiri Soufi ◽  
Ali Akbar Poursadegh Zonouzi ◽  
Ebrahim Eftekhar ◽  
Kamila Kamali ◽  
Sara Aghakhani Chegeni ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Umbilical Vein ◽  
Control Group ◽  
Human Umbilical Vein ◽  
Expression Levels ◽  
Expression Of Genes ◽  
Mirnas Expression ◽  
Umbilical Vein Endothelial Cells ◽  
Mrna Expression Levels

AbstractObjectives. It has been shown that dysregulation of miRNAs expression contributes to the pathogenesis and progression of the diabetes and diabetes-related complications. Drosha, DGCR8, Dicer, and Ago-2 are involved in the miRNA maturation. The aim of the present study was to investigate the mRNA expression levels of these genes in the human umbilical vein endothelial cells (HUVECs) under hyperglycemic condition.Methods. HUVECs were cultured in normo-(5 mM) and hyperglycemic (25 mM) conditions for 24 h. As osmotic control, cells were treated with D-mannitol (25 mM, for 24 h). The mRNA expression levels of Drosha, DGCR8, Dicer and Ago-2 were evaluated using quantitative real-time PCR.Results. The expression level of Drosha, DGCR8, Dicer, and Ago-2 were increased in hyperglycemic HUVECs compared to the control group.Conclusion. Our results show that under hyperglycemic condition, expression of genes involved in the miRNA maturation was significantly increased in HUVECs. Upregulation of these genes may have role in diabetic complications through the dysregulation of the miRNA expression.

scholarly journals A Randomised, Controlled Study of Different Glycaemic Targets during Gestational Diabetes Treatment: Effect on the Level of Adipokines in Cord Blood and ANGPTL4 Expression in Human Umbilical Vein Endothelial Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
P. Popova ◽  
L. Vasilyeva ◽  
A. Tkachuck ◽  
M. Puzanov ◽  
A. Golovkin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Gestational Diabetes ◽  
Cord Blood ◽  
Umbilical Vein ◽  
Fasting Blood Glucose ◽  
Controlled Study ◽  
Control Group ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Our aim was to study the expression of adipokine-encoding genes (leptin, adiponectin, and angiopoietin-like protein 4 (ANGPTL4)) in human umbilical vein endothelial cells (HUVECs) and adipokine concentration in cord blood from women with gestational diabetes mellitus (GDM) depending on glycaemic targets. GDM patients were randomised to 2 groups per target glycaemic levels: GDM1 (tight glycaemic targets, fasting blood glucose < 5.1 mmol/L and <7.0 mmol/L postprandial, N=20) and GDM2 (less tight glycaemic targets, <5.3 mmol/L and < 7.8 mmol/L, respectively, N=21). The control group included 25 women with normal glucose tolerance. ANGPTL4 expression was decreased in the HUVECs from GDM patients versus the control group (23.11 ± 5.71, 21.47 ± 5.64, and 98.33 ± 20.92, for GDM1, GDM2, and controls; p<0.001) with no difference between GDM1 and GDM2. The level of adiponectin gene expression was low and did not differ among the groups. Leptin gene expression was undetectable in HUVECs. In cord blood, leptin/adiponectin ratio (LAR) was increased in GDM2 compared to controls and GDM1 (p=0.038) and did not differ between GDM1 and controls. Tight glycaemic targets were associated with normalisation of increased LAR in the cord blood. ANGPTL4 expression was downregulated in HUVECs of newborns from GDM mothers and was not affected by the intensity of glycaemic control.

scholarly journals Sevoflurane inhibits Human umbilical vein endothelial cells migration by up-regulating VE-cadherin expression

2020 ◽  
Author(s):  
Yuanqing Sun ◽  
Zifeng Xu ◽  
Tao Xu ◽  
Hui Xu
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Control Group ◽  
Vascular Endothelial ◽  
Minimal Alveolar Concentration ◽  
Migration Distance ◽  
Inhalation Anesthesia ◽  
Human Umbilical Vein ◽  
Significant Difference ◽  
Umbilical Vein Endothelial Cells

Abstract Background Sevoflurane is a commonly used inhalation anesthesia and is famous for rapid onset of action, less metabolism in vivo and fast recovery. The aim of this study is to elaborate whether sevoflurane inhibits Human umbilical vein endothelial cells (HUVECs) migration function.Methods In vitro experiments, the HUVECs were divided into four groups randomly, and were exposed to 2% sevoflurane, refer to 1.6 minimal alveolar concentration (MAC), respectively for 0.5h, 1h, 2h and the first group was the control group which exposed to the same gas environment with other three groups but only without sevoflurane. After sevoflurane exposure, HUVECs were conducted the scratch assay.Results The results suggested that the HUVECs exposed to 2% sevoflurane for 2 h were more obviously inhibited on the migration distance during 12 h after scratched than the control group. Quantitative PCR results suggested that the HUVECs exposed to 2% sevoflurane for 2 h expressed more vascular endothelial cadherin (VE-cadherin) than the control group, with statistic difference. However, other scratch assay and quantitative trials suggested that the HUVECs which were transfected with VE-cadherin siRNA and exposed to 2% sevoflurane for 2 h had no significant difference with the control group on the migration distance and the expression of VE-cadherin.Conclusion These results suggested that sevoflurane inhibited the HUVECs migration function by up-regulating VE-cadherin expression, and may have an adverse effect on the normal functions of vascular endothelial cells.

scholarly journals miR-1273g-3p participates in acute glucose fluctuation-induced autophagy, dysfunction, and proliferation attenuation in human umbilical vein endothelial cells

2016 ◽  
Vol 310 (9) ◽  
pp. E734-E743 ◽  
Author(s):  
Jun Guo ◽  
Yaxiong Sang ◽  
Tao Yin ◽  
Bo Wang ◽  
Wenping Yang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Critically Ill ◽  
High Mortality ◽  
Critically Ill Patients ◽  
Umbilical Vein ◽  
Control Group ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Acute glucose fluctuations (AGF) often cause high mortality among critically ill patients, but the mechanisms induced by AGF are not clear. Recent studies suggest that endothelial dysfunction is a key factor that leads to high mortality among critically ill patients. Our goal is to evaluate the phenomenon and mechanisms of endothelial dysfunction induced by AGF. In this study, the functions of human umbilical vein endothelial cells (HUVECs) were compared after treatment with sustained high glucose (SHG), AGF in two groups (AGF1 fluctuations between 5 and 16 mM and AGF2 fluctuations between 5 and 25 mM), and normal glucose levels as a control group (CTR). The medium of the groups was changed every 4 h. The influence of AGF on wound healing was also tested on C57BL/6 mice. The results show that cell proliferation, angiogenesis, and migration functions were injured in the SHG and both AGF groups. AGF2 group shows the worse condition in vitro. In vivo, the wound healing was delayed after the AGF treatment. Furthermore, the markers of apoptosis and autophagy were analyzed. We observed that the autophagy changed in all treatment groups, but apoptosis showed no change. To get to know the mechanism of dysfunction and autophagy, we performed the microRNA chip assay and real-time PCR and found miR-1273g-3p remarkably changed in AGF2 group. After the mimic and inhibitor of miR-1273g-3p were transfected during the AGF2 treatment, we found that the dysfunction and autophagy were partially enhanced by miR-1273g-3p mimic and reversed by miR-1273g-3p inhibitor in AGF2 group. Thus, we conclude that AGF can induce more dysfunction and autophagy, and miR-1273g-3p is also an important factor that leads to the injury.

scholarly journals PPAR-αAgonist Fenofibrate Upregulates Tetrahydrobiopterin Level through Increasing the Expression of Guanosine 5′-Triphosphate Cyclohydrolase-I in Human Umbilical Vein Endothelial Cells

PPAR Research ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jinbo Liu ◽  
Changlin Lu ◽  
Fuwang Li ◽  
Haining Wang ◽  
Liyun He ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Peroxisome Proliferator Activated Receptor ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide (NO) synthase. Guanosine 5′-triphosphate cyclohydrolase-I (GTPCH-I) is a key limiting enzyme for BH4 synthesis. In the present in vitro study, we investigated whether peroxisome proliferator-activated receptorα(PPAR-α) agonist fenofibrate could recouple eNOS by reversing low-expression of intracellular BH4 in endothelial cells and discussed the potential mechanisms. After human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS) for 24 hours, the levels of cellular eNOS, BH4 and cell supernatant NO were significantly reduced compared to control group. And the fluorescence intensity of intracellular ROS was significantly increased. But pretreated with fenofibrate (10 umol/L) for 2 hours before cells were induced by LPS, the levels of eNOS, NO, and BH4 were significantly raised compared to LPS treatment alone. ROS production was markedly reduced in fenofibrate group than LPS group. In addition, our results showed that the level of intracellular GTPCH-I detected by western blot was increased in a concentration-dependent manner after being treated with fenofibrate. These results suggested that fenofibrate might help protect endothelial function and against atherosclerosis by increasing level of BH4 and decreasing production of ROS through upregulating the level of intracellular GTPCH-I.

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