scholarly journals Hsa_circ_0004831 downregulation is partially responsible for atorvastatinalleviated human umbilical vein endothelial cell injuries induced by ox-LDL through targeting the miR-182-5p/CXCL12 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Gang Su ◽  
Guangli Sun ◽  
Jian Lv ◽  
Weiwei Zhang ◽  
Hai Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Viability ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Luciferase Reporter ◽  
Cycle Progression ◽  
Human Umbilical Vein

Abstract Background The dysfunction and injury of human umbilical vein endothelial cells (HUVECs) are key events of atherosclerosis (AS). Atorvastatin (ATV) has been shown to play a protective role on endothelial cells. However, the associated molecular mechanisms remain not fully illustrated. Methods HUVECs were treated with oxidized low-density lipoprotein (ox-LDL) to mimic the pathological conditions of endothelial cell injury in AS. Cell injuries were assessed according to cell viability, cell apoptosis, cycle progression, oxidative stress and inflammatory responses using CCK-8 assay, flow cytometry assay or commercial kits. The expression of hsa_circ_0004831, miR-182-5p, and C-X-C motif chemokine 12 (CXCL12) mRNA was examined using quantitative real-time PCR (qPCR). The expression of CXCL12 protein was quantitated by western blot. The predicted target relationship between miR-182-5p and hsa_circ_0004831 or CXCL12 was verified by pull-down assay, dual-luciferase reporter assay or RIP assay. Results The expression of hsa_circ_0004831 was upregulated by ox-LDL but downregulated by ATV in HUVECs. ATV promoted cell viability and cell cycle progression but inhibited apoptosis, oxidative stress and inflammation in ox-LDL-treated HUVECs, while the role of ATV was partially reversed by hsa_circ_0004831 overexpression. MiR-182-5p was targeted by hsa_circ_0004831, and hsa_circ_0004831 overexpression-restored apoptosis, oxidative stress and inflammation were blocked by miR-182-5p restoration. Further, CXCL12 was targeted by miR-182-5p, and miR-182-5p inhibition-stimulated apoptosis, oxidative stress and inflammation were lessened by CXCL12 knockdown. Conclusion Hsa_circ_0004831-targeted miR-182-5p/CXCL12 regulatory network is one of the pathways by which ATV protects against ox-LDL-induced endothelial injuries.

scholarly journals Dietary Nucleotides Retard Oxidative Stress-Induced Senescence of Human Umbilical Vein Endothelial Cells

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3279
Author(s):  
Na Zhu ◽  
Xinran Liu ◽  
Meihong Xu ◽  
Yong Li
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Viability ◽  
Mitochondrial Function ◽  
Umbilical Vein ◽  
Lower Percentage ◽  
Human Umbilical Vein ◽  
Dietary Nucleotides ◽  
Umbilical Vein Endothelial Cells

Several lines of evidence suggest an inhibitory role of dietary nucleotides (NTs) against oxidative stress and inflammation, which promote senescence in age-associated cardiovascular diseases. We sought to test whether the dietary NTs could retard the hydrogen peroxide (H2O2)-induced senescence of human umbilical vein endothelial cells (HUVECs) and to elucidate the efficiency of different NTs as well as the potential mechanism. Senescence was induced in HUVECs by 4 h exposure to 200 µM H2O2 and was confirmed using senescence-associated-β-galactosidase staining (SA-β-gal), cell viability, and Western blot analyses of p16INK4A and p21Waf1/Cip1 after 24 h administration of growth medium. We find that NTs retards oxidative stress-induced HUVECs senescence, as shown by a lower percentage of SA-β-gal-positive cells, lower expression of p16INK4A, and p21Waf1/Cip1 as well as higher cell viability. GMP100 was the most excellent in delaying HUVECs senescence, which was followed by the NTs mixture, NMN, CMP50, and UMP50/100, while AMP retards HUVECs senescence by specifically reducing p15INK4b expression. NTs all have significant anti-inflammatory effects; AMP and CMP were more prominent in restoring mitochondrial function, GMP and CMP were more competent at eliminating ROS and MDA, while AMP and UMP were more efficient at enhancing antioxidant enzyme activity. The role of the NTs mixture in retarding HUVECs senescence is full-scaled. These results stated that the mechanisms of NTs retarding HUVECs senescence could be related to its antioxidant and anti-inflammation properties promoting cell proliferation and protecting mitochondrial function activities.

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.

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 LPS promotes the progression of sepsis by activation of lncRNA HULC/miR-204-5p/TRPM7 network in HUVECs

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xinghai Chen ◽  
Debiao Song
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cell Viability ◽  
Transient Receptor Potential ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Receptor Potential ◽  
Luciferase Reporter ◽  
Inflammatory Injury ◽  
And Oxidative Stress

Abstract Sepsis is a systemic inflammatory response syndrome caused by infection. Lipopolysaccharide (LPS) has been reported to induce inflammatory responses, and long non-coding RNA highly up-regulated in liver cancer (HULC) expression was associated with the progression of sepsis. But the role and underlying mechanism of HULC in LPS-induced sepsis remain unclear. Cell viability and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) and flow cytometry assays, respectively. The levels of apoptosis-related proteins, inflammatory cytokines and transient receptor potential melastatin7 (TRPM7) were detected by western blot. Reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were detected by dichloro-dihydro-fluorescein diacetate (DCFH-DA) method using commercial kit. HULC, microRNA-204-5p (miR-204-5p) and TRPM7 expressions in serum of sepsis patients and human umbilical vein endothelial cells (HUVECs) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between HULC and miR-204-5p, miR-204-5p and TRPM7. LPS stimulation restrained cell viability and facilitated apoptosis, inflammatory injury and oxidative stress in HUVECs. HULC and TRPM7 were increased and accompanied with decreased miR-204-5p expression in serum of sepsis patients. A significant negative correlation between miR-204-5p and HULC or TRPM7 was observed, and there was a positive relationship between expressions of HULC and TRPM7. Importantly, LPS inhibited the cell viability and induced apoptosis, inflammatory injury and oxidative stress of HUVECs by up-regulating the expressions of HULC and TRPM7, and down-modulating miR-204-5p expression. Mechanically, HULC positively regulated TRPM7 expression by sponging miR-204-5p in HUVECs. LPS impaired cell viability, and promoted cell apoptosis, inflammatory response and oxidative stress in HUVECs by regulating HULC/miR-204-5p/TRPM7 axis.

Rhodiola crenulata Attenuates High Glucose Induced Endothelial Dysfunction in Human Umbilical Vein Endothelial Cells

2017 ◽  
Vol 45 (06) ◽  
pp. 1201-1216 ◽  
Author(s):  
Li-Yen Huang ◽  
I-Chuan Yen ◽  
Wei-Cheng Tsai ◽  
Blerina Ahmetaj-Shala ◽  
Tsu-Chung Chang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Cell Viability ◽  
High Glucose ◽  
Umbilical Vein ◽  
Root Extract ◽  
Human Umbilical Vein ◽  
Rhodiola Crenulata ◽  
Umbilical Vein Endothelial Cells

Rhodiola crenulata root extract (RCE), a traditional Chinese medicine, has been shown to regulate glucose and lipid metabolism via the AMPK pathway in high glucose (HG) conditions. However, the effect of RCE on HG-induced endothelial dysfunction remains unclear. The present study was designed to examine the effects and mechanisms of RCE against hyperglycemic insult in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were pretreated with or without RCE and then exposed to 33[Formula: see text]mM HG medium. The cell viability, nitrite production, oxidative stress markers, and vasoactive factors, as well as the mechanisms underlying RCE action, were then investigated. We found that RCE significantly improved cell death, nitric oxide (NO) defects, and oxidative stress in HG conditions. In addition, RCE significantly decreased the HG-induced vasoactive markers, including endothelin-1 (ET-1), fibronectin, and vascular endothelial growth factor (VEGF). However, the RCE-restored AMPK-Akt-eNOS-NO axis and cell viability were abolished by the presence of an AMPK inhibitor. These findings suggested that the protective effects of RCE were associated with the AMPK-Akt-eNOS-NO signaling pathway. In conclusion, we showed that RCE protected endothelial cells from hyperglycemic insult and demonstrated its potential for use as a treatment for endothelial dysfunction in diabetes mellitus.

Serum from healthy pregnant women reduces oxidative stress in human umbilical vein endothelial cells

2002 ◽  
Vol 103 (1) ◽  
pp. 53-57 ◽  
Author(s):  
Fortunato SCALERA ◽  
Tina FISCHER ◽  
Dietmar SCHLEMBACH ◽  
Ernst BEINDER
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Pregnant Women ◽  
Reduced Glutathione ◽  
Umbilical Vein ◽  
Lipid Peroxides ◽  
Human Endothelial Cells ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

This study was conducted to compare the effects of serum from healthy pregnant women and that from pregnant women with pre-eclampsia on oxidative stress in endothelial cells in culture. Human umbilical vein endothelial cells (HUVECs) were incubated with serum from 18 pre-eclamptic, 18 healthy pregnant and 18 healthy non-pregnant women for 24h. The levels of reduced glutathione (GSH) and lipid peroxides (LPOs) were measured in endothelial cell lysates. Measurement of malondialdehyde in combination with 4-hydroxyalkenals has been used as an indicator of LPOs. Serum from healthy pregnant women decreased significantly the LPO content in HUVECs in comparison with serum from pre-eclamptic women and healthy non-pregnant women (30.7±6.6 compared with 39.3±10.9 and 41.0±12.7pmol/mg of protein respectively; P<0.003 and P<0.01 respectively). No differences in GSH content between the three groups (18.3±2.1nmol/mg of protein for healthy pregnant, 19.2±3.3nmol/mg for pre-eclamptic and 18.3±2.0nmol/mg for healthy non-pregnant women) were found. Thus serum from normal pregnant women contains a factor(s) that decreases oxidative stress in human endothelial cells. This mechanism might be altered in pre-eclampsia.

scholarly journals Cytoprotective Peptides from Blue Mussel Protein Hydrolysates: Identification and Mechanism Investigation in Human Umbilical Vein Endothelial Cells Injury

Marine Drugs ◽  
2021 ◽  
Vol 19 (11) ◽  
pp. 609
Author(s):  
Indyaswan Tegar Suryaningtyas ◽  
Chang-Bum Ahn ◽  
Jae-Young Je
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Molecular Mechanisms ◽  
Blue Mussel ◽  
Umbilical Vein ◽  
Ros Generation ◽  
Heme Oxygenase 1 ◽  
Human Umbilical Vein ◽  
Bax Protein ◽  
Umbilical Vein Endothelial Cells

Cardiovascular disease represents a leading cause of mortality and is often characterized by the emergence of endothelial dysfunction (ED), a physiologic condition that takes place in the early progress of atherosclerosis. In this study, two cytoprotective peptides derived from blue mussel chymotrypsin hydrolysates with the sequence of EPTF and FTVN were purified and identified. Molecular mechanisms underlying the cytoprotective effects against oxidative stress which lead to human umbilical vein endothelial cells (HUVEC) injury were investigated. The results showed that pretreatment of EPTF, FTVN and their combination (1:1) in 0.1 mg/mL significantly reduced HUVEC death due to H2O2 exposure. The cytoprotective mechanism of these peptides involves an improvement in the cellular antioxidant defense system, as indicated by the suppression of the intracellular ROS generation through upregulation of the cytoprotective enzyme heme oxygenase-1. In addition, H2O2 exposure triggers HUVEC damage through the apoptosis process, as evidenced by increased cytochrome C release, Bax protein expression, and the elevated amount of activated caspase-3, however in HUVEC pretreated with peptides and their combination, the presence of those apoptotic stimuli was significantly decreased. Each peptide showed similar cytoprotective effect but no synergistic effect. Taken together, these peptides may be especially important in protecting against oxidative stress-mediated ED.

scholarly journals Knockdown of circ_0003204 alleviates oxidative low-density lipoprotein-induced human umbilical vein endothelial cells injury: Circulating RNAs could explain atherosclerosis disease progression

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 558-569
Author(s):  
Qiuxia Su ◽  
Xianhua Dong ◽  
Chonghui Tang ◽  
Xiaojie Wei ◽  
Youguo Hao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Luciferase Reporter ◽  
Low Density ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Abstract Atherosclerosis (AS) is a serious cardiovascular disease. Circular RNAs (circRNAs) play an important role in the progression of many diseases, including AS. However, the role of circ_0003204 in AS is not clear. Oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) were used to construct an AS cell model in vitro. Cell viability was assessed using cell counting kit 8 (CCK8) assay. Flow cytometry and caspase-3 activity were used to measure cell apoptosis. The contents of inflammatory cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Oxidative stress marker expression and cell injury marker activity were detected by their corresponding Assay Kits. Besides, the expression levels of circ_0003204, miR-330-5p, and toll-like receptor 4 (TLR4) were tested by real-time polymerase chain reaction (qPCR). The interaction between miR-330-5p and circ_0003204 or TLR4 was examined by dual-luciferase reporter assay and RNA pull-down assay. Western blot (WB) analysis was used to determine the levels of TLR4 protein and nuclear factor-kappa B (NF-κB) signaling pathway-related protein. Our data suggested that ox-LDL could suppress viability and promote apoptosis, inflammatory response, and oxidative stress in HUVECs. circ_0003204 was highly expressed in ox-LDL-induced HUVECs, and its silencing could inhibit ox-LDL-induced HUVECs injury. miR-330-5p could be sponged by circ_0003204, and its inhibitor could reverse the inhibition effect of silenced circ_0003204 on ox-LDL-induced HUVECs injury. Further, TLR4 could be targeted by miR-330-5p, and its overexpression could invert the suppression effect of miR-330-5p on ox-LDL-induced HUVECs injury. The activity of the NF-κB signaling pathway was regulated by the circ_0003204/miR-330-5p/TLR4 axis. Our results indicated that circ_0003204 silencing could alleviate ox-LDL-induced HUVECs injury, suggesting that circ_0003204 might be a novel target for AS treatment.

scholarly journals Cytoprotective Role of Edible Seahorse (Hippocampus abdominalis)-Derived Peptides in H2O2-Induced Oxidative Stress in Human Umbilical Vein Endothelial Cells

Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 86
Author(s):  
Yunok Oh ◽  
Chang-Bum Ahn ◽  
Jae-Young Je
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Combination Treatment ◽  
Umbilical Vein ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Staining ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Oxidative stress-induced endothelial dysfunction is strongly linked to the pathogenesis of cardiovascular diseases. A previous study revealed that seahorse hydrolysates ameliorated oxidative stress-mediated human umbilical vein endothelial cells (HUVECs) injury. However, the responsible compounds have not yet been identified. This study aimed to identify cytoprotective peptides and to investigate the molecular mechanism underlying the cytoprotective role in H2O2-induced HUVECs injury. After purification by gel filtration and HPLC, two peptides were sequenced by liquid chromatography-tandem mass spectrometry as HGSH (436.43 Da) and KGPSW (573.65 Da). The synthesized peptides and their combination (1:1 ratio) showed significant HUVECs protection effect at 100 μg/mL against H2O2-induced oxidative damage via significantly reducing intracellular reactive oxygen species (ROS). Two peptides and their combination treatment resulted in the increased heme oxygenase-1 (HO-1), a phase II detoxifying enzyme, through the activation of nuclear transcription factor-erythroid 2-related factor (Nrf2). Additionally, cell cycle and nuclear staining analysis revealed that two peptides and their combination significantly protected H2O2-induced cell death through antiapoptotic action. Two peptides and their combination treatment led to inhibit the expression of proapoptotic Bax, the release of cytochrome C into the cytosol, the activation of caspase 3 by H2O2 treatment in HUVECs, whereas antiapoptotic Bcl-2 expression was increased with concomitant downregulation of Bax/Bcl-2 ratio. Taken together, these results suggest that seahorse-derived peptides may be a promising agent for oxidative stress-related cardiovascular diseases.

Sign in / Sign up

Export Citation Format

Share Document