scholarly journals The role of 4-pba on tnf-alpha related apoptosis on human vein endothelial cells

2019 ◽  
Vol 18 (2) ◽  
pp. 391-394
Author(s):  
Oski Illiandri
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Medical Science ◽  
Degenerative Disease ◽  
Control Group ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells ◽  
Study Laboratory

Tumor Necrotizing Factor-alpha (TNF-α) has been well-known as a potent pro-inflamatory cytokine involved in many degenerative disease. Oneof its primary target organ-damaged wasendothelial cellswhich willlead to its endoplasmic reticulum stress (ERS) and induced its apoptosis. Endothelial cell apoptosis will lead high implication in many disease pathomechanism ofmany degenerative disease. Some study report ERS inhibitor 4-Phenyl Butyric Acid (4-PBA) properties to inhibitinflammation processin endothelial cells.However, wether 4-PBA can decrease apoptosis level in inflamationof endothelial cells is still poorly understood Objective. This study to answer whether 4-PBA can decrease apoptosis triggered by inflammatory reactions mediated by TNFα. Methods: This study is an exploratory study laboratory in vitro using cell culture Human Umbilical Vein Endothelial Cells (HUVEC) apoptotic count cells with the design of post test only control group consisting of three treatment groups with doses of 4-PBA 1 nM / mL, 2 nM /mL, and 3 nM /m L. Results. Administration4-PBA in cultured HUVEC derived endothelial cells significantly decrease apoptosis at any dose of PBA but no dose dependently (p <0.05) Conclusion: Based on the results that has been done, it can be concluded that 4-PBA can reduce levels of endothelial cells apoptosis which were exposed to proinflamatory cytokine TNF-α. Further research need to elucidated 4-PBA mechanism to inhibit endothelial apoptosis. Bangladesh Journal of Medical Science Vol.18(2) 2019 p.391-394

Endothelial CSN5 impairs NF-κB activation and monocyte adhesion to endothelial cells and is highly expressed in human atherosclerotic lesions

2013 ◽  
Vol 110 (07) ◽  
pp. 141-152 ◽  
Author(s):  
Yaw Asare ◽  
Erdenechimeg Shagdarsuren ◽  
Johannes Schmid ◽  
Pathricia Tilstam ◽  
Jochen Grommes ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Negative Regulator ◽  
Multifunctional Protein ◽  
Atherosclerotic Lesions ◽  
Tnf Α ◽  
Reporter Assays ◽  
Umbilical Vein Endothelial Cells

SummaryThe COP9 signalosome (CSN), a multifunctional protein complex involved in the regulation of cullin-RING-E3 ubiquitin ligases (CRLs), has emerged as a regulator of NF-κB signalling. As NF-κB drives the expression of pro-inflammatory and pro-atherosclerotic genes, we probed the yet unknown role of the CSN, in particular CSN5, on NF-KB-mediated atherogenic responses in endothelial cells. Co-immunoprecipitation in human umbilical vein endothelial cells (HUVECs) revealed the presence of a super-complex between IKK and CSN, which dissociates upon TNF-α stimulation. Furthermore, CSN5 silencing enhanced TNF-α-induced IKB-α degradation and NF-κB activity in luci-ferase reporter assays. This was paralleled by an increased NF-KB-driven upregulation of atherogenic chemokines and adhesion molecules, as measured by qPCR and flow cytometry, and translated into an enhanced arrest of THP-1 monocytes on TNF-α-stimulated, CSN5-depleted HUVECs. Reverse effects on NF-κB activity and THP-1 arrest were seen upon CSN5 overexpression. Finally, double-immunostaining confirmed the expression of CSN subunits in the endothelium of human atherosclerotic lesions, and revealed an increased expression of CSN5 which correlated with atheroprogression. In conclusion, endothelial CSN5 attenuates NF-KB-dependent pro-inflammatory gene expression and monocyte arrest on stimulated endothelial cells in vitro, suggesting that CSN5 might serve as a negative regulator of atherogenesis.Note: The review process for this manuscript was fully handled by G. Y. H. Lip, Editor in Chief.

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.

The Effects of Carnosine on High Glucose-Induced Apoptosis of Human Umbilical Vein Endothelial Cells

2011 ◽  
Vol 345 ◽  
pp. 365-369
Author(s):  
Yan Shi ◽  
Chun Jing Zhang
Keyword(s):  
Electron Microscopy ◽  
Flow Cytometry ◽  
Endothelial Cells ◽  
High Glucose ◽  
Umbilical Vein ◽  
Control Group ◽  
Human Umbilical Vein ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

.Purposes,To explore the effects of carnosine on high glucose-induced apoptosis of human umbilical vein endothelial cells (HUVECs). Methods HUVECs were cultured in vitro. The cellular apoptotic model was made by the addition of high glucose (25 mmol/L), the group of high glucose and carnosine was administered by the addition of high glucose (25 mmol/L) with carnosine (20 mmol/L). In addition, cell apoptosis was detected by the electron microscopy and AnnexinV/PI flow cytometry. Results Compared with the control group, high glucose could induce HUVECs apoptosis under electron microscopy and AnnexinV/PI flow cytometry, while 20 mmol/L carnosine could inhibit the apoptosis induced by high glucose significantly (##P <0.05). Conclusion In this study, carnosine could inhibit high-glucose induced apoptosis of human umbilical vein endothelial cells.

scholarly journals In vitro ability of Staphylococcus aureus isolates from bacteraemic patients with and without metastatic complications to invade vascular endothelial cells

2007 ◽  
Vol 56 (10) ◽  
pp. 1290-1295 ◽  
Author(s):  
Wan Beom Park ◽  
Sung Han Kim ◽  
Cheol-in Kang ◽  
Jae Hyun Cho ◽  
Ji Whan Bang ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Control Group ◽  
Vascular Endothelial ◽  
Tertiary Referral Hospital ◽  
Metastatic Infection ◽  
Umbilical Vein Endothelial Cells

Invasion of vascular endothelial cells is thought to be a critical step in the development of metastatic infections in patients with Staphylococcus aureus bacteraemia. This study was designed to evaluate the association between the ability to invade endothelial cells and metastatic infection by S. aureus. Patients with metastatic infection were identified among those with community-acquired S. aureus bacteraemia in a tertiary referral hospital. Patients with simple bacteraemia caused by S. aureus over the same period served as the control group. The ability of each clinical isolate to invade endothelial cells was evaluated by counting the number of intracellular organisms 1 h after inoculation onto human umbilical vein endothelial cells in vitro. The cytotoxic activity of intracellular S. aureus was determined 24 h after internalization, and expressed as the percentage of cells killed. The clinical isolates varied in invasiveness and cytotoxicity. The median invasiveness, relative to S. aureus reference strain ATCC 29213, was 145  % in the cases (n=10) [interquartile range (IQR) 103–160] and 153  % (IQR 111–173) in the controls (n=11; P=0.44). The median cytotoxicity was 59.4  % (IQR 47–68) in the cases and 65.2  % (IQR 50–74) in the controls (P=0.44). Differences in the ability of S. aureus to invade and destroy vascular endothelial cells in vitro were not associated with the development of metastatic complications in patients with S. aureus bacteraemia. This implies that the invasiveness and toxicity of S. aureus for endothelial cells may not be major determinants of metastatic infection.

scholarly journals Comparison of cytotoxicity of vascular prostheses in vitro

2020 ◽  
Vol 28 (2) ◽  
pp. 183-192
Author(s):  
Roman E. Kalinin ◽  
Igor A. Suchkov ◽  
Nina D. Mzhavanadze ◽  
Natalya V. Korotkova ◽  
Aleksandr A. Nikiforov ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Polyethylene Terephthalate ◽  
Metabolic Activity ◽  
Umbilical Vein ◽  
Control Group ◽  
Vascular Prostheses ◽  
Mean Values ◽  
Microplate Reader ◽  
Umbilical Vein Endothelial Cells

Aim. To study and compare cytotoxicity of the main types of synthetic prostheses used in arterial reconstructive surgery, including polytetrafluoroethylene (PTFE) and polyethylene-terephthalate (Dacron). Materials and Methods. On the culture of human umbilical vein endothelial cells (HUVEC) of the 3rd passage, MTS test was conducted that is used in laboratory examinations with attraction of cellular technologies to study cytotoxicity of medical drugs and medical products. The test implies use of MTS reagent that is 3-(4,5-dimethylthiazol-2-il)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; additionally phenazine methosulfate (PMS) was used that plays the role of electron-binding reagent. In the experiment, cells were incubated with PTFE and Dacron within 24 hours at 37ᵒC with 5% CO2. For control, HUVEC cultured in the standard growth medium, were used. In the presence of PMS, MTS was reduced by mitochondrial dehydrogenases of endothelial cells to formazan staining blue. Supernatant of cell cultures was evaluated by photocolorimetric method on Stat Fax 3200 analyzer (microplate reader) of Awareness technology Inc. Palm City Fl. (USA). Results. The lowest mean values were noted in Dacron group 0.21 (0.20-0.22) optical density units, the highest values were noted in the control group 0.36 (0.35-0.38); parameters in PTFE group were 0.35 (0.33-0.36). In comparison of the groups statistically significant differences were found between the control group and Dacron group (р0.001), control and PTFE group (р=0.037), Dacron and PTFE (р0.001). Incubation with Dacron led to suppression of metabolic activity of cells by 41.7% as compared to the control group (р0.001). Metabolic activity of cells exposed to PTFE, approached that of the control group, that is, it corresponded to the optimal conditions of culturing of endothelial cells in vitro. Conclusion. In comparison with polyethylene-terephthalate (Dacron), polytetrafluoro-ethylene (PTFE) showed the least suppression of metabolic activity of endothelial cells in vitro.

scholarly journals Lycopene inhibits angiogenesis in human umbilical vein endothelial cells and rat aortic rings

2011 ◽  
Vol 108 (3) ◽  
pp. 431-439 ◽  
Author(s):  
Simone Elgass ◽  
Alan Cooper ◽  
Mridula Chopra
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Inhibitory Effect ◽  
Human Umbilical Vein ◽  
Promising Target ◽  
Tnf Α ◽  
Tumour Vascularisation ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Growth Factor

Angiogenesis is important for tumour vascularisation and growth, and is therefore a promising target for cancer therapy. The present study reports inhibition ofin vitroangiogenesis in human umbilical vein endothelial cells (HUVEC) as well as in rat aortic rings at physiological concentrations of lycopene, that is, 1–2 μmol/l. At a final concentration of 1·15 μmol/l, a significant reduction (P < 0·05) in network branching, that is, junction numbers, the number of tubules and tubule length, was observed in both HUVEC as well as in the rat aortic rings. The inhibitory effect of lycopene was independent of the presence of the pro-angiogenic agents, vascular endothelial growth factor and TNF-α. The anti-angiogenic effects of lycopene in the present study were shown at a concentration that should be achievable by dietary means. These results extend our knowledge of one of the putative anti-cancer actions of lycopene.

scholarly journals Generation of a Novel In Vitro Model to Study Endothelial Dysfunction from Atherothrombotic Specimens

2021 ◽  
Author(s):  
Susan Gallogly ◽  
Takeshi Fujisawa ◽  
John D. Hung ◽  
Mairi Brittan ◽  
Elizabeth M. Skinner ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
In Vitro Model ◽  
Umbilical Vein ◽  
Coronary Syndrome ◽  
Coronary Endothelial Cells ◽  
Vitro Model ◽  
Umbilical Vein Endothelial Cells

Abstract Purpose Endothelial dysfunction is central to the pathogenesis of acute coronary syndrome. The study of diseased endothelium is very challenging due to inherent difficulties in isolating endothelial cells from the coronary vascular bed. We sought to isolate and characterise coronary endothelial cells from patients undergoing thrombectomy for myocardial infarction to develop a patient-specific in vitro model of endothelial dysfunction. Methods In a prospective cohort study, 49 patients underwent percutaneous coronary intervention with thrombus aspiration. Specimens were cultured, and coronary endothelial outgrowth (CEO) cells were isolated. CEO cells, endothelial cells isolated from peripheral blood, explanted coronary arteries, and umbilical veins were phenotyped and assessed functionally in vitro and in vivo. Results CEO cells were obtained from 27/37 (73%) atherothrombotic specimens and gave rise to cells with cobblestone morphology expressing CD146 (94 ± 6%), CD31 (87 ± 14%), and von Willebrand factor (100 ± 1%). Proliferation of CEO cells was impaired compared to both coronary artery and umbilical vein endothelial cells (population doubling time, 2.5 ± 1.0 versus 1.6 ± 0.3 and 1.2 ± 0.3 days, respectively). Cell migration was also reduced compared to umbilical vein endothelial cells (29 ± 20% versus 85±19%). Importantly, unlike control endothelial cells, dysfunctional CEO cells did not incorporate into new vessels or promote angiogenesis in vivo. Conclusions CEO cells can be reliably isolated and cultured from thrombectomy specimens in patients with acute coronary syndrome. Compared to controls, patient-derived coronary endothelial cells had impaired capacity to proliferate, migrate, and contribute to angiogenesis. CEO cells could be used to identify novel therapeutic targets to enhance endothelial function and prevent acute coronary syndromes.

scholarly journals Effect of TNFα stimulation on expression of kidney risk inflammatory proteins in human umbilical vein endothelial cells cultured in hyperglycemia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zaipul I. Md Dom ◽  
Caterina Pipino ◽  
Bozena Krolewski ◽  
Kristina O’Neil ◽  
Eiichiro Satake ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Systemic Exposure ◽  
In Vitro Study ◽  
Human Umbilical Vein ◽  
Intracellular Fraction ◽  
Inflammatory Proteins ◽  
Umbilical Vein Endothelial Cells ◽  
Extracellular Fraction

AbstractWe recently identified a kidney risk inflammatory signature (KRIS), comprising 6 TNF receptors (including TNFR1 and TNFR2) and 11 inflammatory proteins. Elevated levels of these proteins in circulation were strongly associated with risk of the development of end-stage kidney disease (ESKD) during 10-year follow-up. It has been hypothesized that elevated levels of these proteins in circulation might reflect (be markers of) systemic exposure to TNFα. In this in vitro study, we examined intracellular and extracellular levels of these proteins in human umbilical vein endothelial cells (HUVECs) exposed to TNFα in the presence of hyperglycemia. KRIS proteins as well as 1300 other proteins were measured using the SOMAscan proteomics platform. Four KRIS proteins (including TNFR1) were down-regulated and only 1 protein (IL18R1) was up-regulated in the extracellular fraction of TNFα-stimulated HUVECs. In the intracellular fraction, one KRIS protein was down-regulated (CCL14) and 1 protein was up-regulated (IL18R1). The levels of other KRIS proteins were not affected by exposure to TNFα. HUVECs exposed to a hyperglycemic and inflammatory environment also showed significant up-regulation of a distinct set of 53 proteins (mainly in extracellular fraction). In our previous study, circulating levels of these proteins were not associated with progression to ESKD in diabetes.

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