Abstract 5078: Physical Training Reduces the Ability of Serum from Patients with Heart Failure to Induce Endothelial Cell Death

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Caterina Mammi ◽  
Massimiliano Caprio ◽  
Stefania Gorini ◽  
Andrea la Sala ◽  
Antonella Antelmi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endothelial Cells ◽  
Cell Death ◽  
Cardiac Rehabilitation ◽  
Physical Training ◽  
Umbilical Vein ◽  
Apoptotic Pathway ◽  
Patients With Heart Failure ◽  
Huvec Cells ◽  
Umbilical Vein Endothelial Cells

Physical training improves endothelial function and exercise capacity in patients with heart failure (HF). Serum from patients with cardiovascular diseases shows increased ability to induce apoptosis in human endothelial cells potentially contributing to the progression of atherosclerotic and endothelial dysfunction. Aim of this study was to evaluate the effect of cardiac rehabilitation on the pro-apoptotic properties of serum in patients with heart failure. Human Umbilical Vein Endothelial Cells (HUVECs) were incubated with 20% serum from 24 patients with HF (HYHA II) before and after cardiovascular rehabilitation. For apoptosis quantification, fragmented DNA was determined using Cell Death detection ELISA kit and propidium iodide (PI) staining analyzed by flow cytometry. The expression on endothelial cells of proteins involved in apoptotic pathway (bax, caspasi-3, bcl-2) was studied by Western blot analysis. Necrosis was evaluated measuring the lactate dehydrogenase released from damaged cells into the supernatant using a cytotoxicity detection kit. Serum from patients with heart failure showed a significantly greater ability to induce apoptosis (67 ± 4,6% vs 23 ± 5,2%, p<0,001) and necrosis (44 ± 3% vs 32 ± 2,1%, p<0,05) of HUVEC cells compared with controls. Cardiac rehabilitation significantly reduced the ability of patient serum to induce apoptosis (PI: 40.44% ± 3,9 vs 25.22% ± 2,6, p<0,01; ELISA: 67 ± 4,6% vs 42 ± 4,4%, p<0,001) and necrosis (44 ± 3% vs 33 ± 2%, p<0,01) of HUVEC cells compared to baseline. Moreover endothelial cells treated with serum after rehabilitation showed a significant decrease of bax expression (1,12 ± 0,06 vs 0,89 ± 0,08, p<0,05) and a significant decrease of cleaved Caspase-3 expression (0,91 ± 0,16 vs 0,72 ± 0,08, p<0.05). Serum of patients with heart failure has increased pro-apoptotic properties. Physical training reduces the ability of serum-contained factors to induce cell death of endothelial cells in patient with heart failure.

Lipid mediators of autophagy in stress-induced premature senescence of endothelial cells

2008 ◽  
Vol 294 (3) ◽  
pp. H1119-H1129 ◽  
Author(s):  
Susann Patschan ◽  
Jun Chen ◽  
Alla Polotskaia ◽  
Natalja Mendelev ◽  
Jennifer Cheng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Umbilical Vein ◽  
Acid Sphingomyelinase ◽  
Premature Senescence ◽  
Human Umbilical Vein ◽  
Glycation End Products ◽  
Umbilical Vein Endothelial Cells ◽  
Stress Induced Premature Senescence

Our group (Patschan S, Chen J, Gealekman O, Krupincza K, Wang M, Shu L, Shayman JA, Goligorsky MS; Am J Physiol Renal Physiol 294: F100–F109, 2008) previously observed an accumulation of gangliosides coincident with development of cell senescence and demonstrated lysosomal permeabilization in human umbilical vein endothelial cells exposed to glycated collagen I (GC). Therefore, we investigated whether the lysosome-dependent, caspase-independent or type 2-programmed cell death (autophagy) is involved in development of premature senescence of endothelial cells. The cleaved microtubule-associated protein 1 light-chain 3 (LC3), a marker of autophagosome formation, was overexpressed within 24 h of GC treatment; however, by 4–5 days, it was nearly undetectable. Early induction of autophagosomes was associated with their fusion with lysosomes, a phenomenon that later became subverted. Autophagic cell death can be triggered by the products of damaged plasma membrane, sphingolipids, and ceramide. We observed a clustering of membrane rafts shortly after exposure to GC; later, after 24 h, we observed an internalization, accompanied by an increased acid sphingomyelinase activity and accumulation of ceramide. Pharmacological inhibition of autophagy prevented development of premature senescence but did lead to the enhanced rate of apoptosis in human umbilical vein endothelial cells exposed to GC. Pharmacological induction of autophagy resulted in reciprocal changes. These observations appear to represent a mechanistic molecular cascade whereby advanced glycation end products like GC induce sphingomyelinase activity, accumulation of ceramide, clustering, and later internalization of lipid rafts.

scholarly journals Curcumin Protects Human Umbilical Vein Endothelial Cells against H2O2-Induced Cell Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Jipeng Ouyang ◽  
Rong Li ◽  
Haiqin Shi ◽  
Jianping Zhong
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Death ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Therapeutic Drug ◽  
Human Umbilical Vein ◽  
Antioxidative Enzyme Activities ◽  
Apoptosis Related Protein ◽  
Umbilical Vein Endothelial Cells

Migraine is a prevalent neurological disorder which causes a huge economic burden on society. It is thought to be a neurovascular disease with oxidative stress might be involved. Curcumin, one of the major ingredients of turmeric, has potent antioxidative and anti-inflammatory properties, but whether it could be used as a potential treatment for migraine remains to be explored. In the present study, human umbilical vein endothelial cells (HUVECs) were pretreated with various concentrations of curcumin (0 μM, 10 μM, 20 μM, 30 μM, 40 μM, and 50 μM) for 12 h, thereby exposed to H2O2 (100 μM) for another 12 h. The viability of HUVECs was tested by the CCK-8 assay, and the activities of antioxidant enzymes including superoxide dismutase (SOD) and glutathione (GSH) were also examined. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were assayed to determine H2O2-induced oxidative stress. In addition, several cell death-related genes (p53, p21, Bax, and Bcl-2) were detected by PCR, and an apoptosis-related protein (caspase3) was evaluated by western blotting. Our results showed that curcumin improved the H2O2-induced decrease of cell viability and antioxidative enzyme activities and decreased the level of oxidative stress. As a conclusion, curcumin could mitigate H2O2-induced oxidative stress and cell death in HUVECs and may be a potential therapeutic drug for migraine.

scholarly journals Photodynamic therapy targeting VCAM-1-expressing human umbilical vein endothelial cells using a PpIX–VCAM-1 binding peptide–quantum dot conjugate

RSC Advances ◽  
2017 ◽  
Vol 7 (80) ◽  
pp. 50562-50570 ◽  
Author(s):  
Huijuan Yin ◽  
Xiafei Shi ◽  
Hong Wang ◽  
Wendong Jin ◽  
Yingxin Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Photodynamic Therapy ◽  
Quantum Dot ◽  
Umbilical Vein ◽  
Photodynamic Effect ◽  
Binding Peptide ◽  
Human Umbilical Vein ◽  
Huvec Cells ◽  
Umbilical Vein Endothelial Cells

Enhanced PDT was induced by the conjugate of PpIX (photodynamic effect)–VCAM-1 binding peptide (target)–QD (carrier) by the augmented ROS on VCAM-1 expressing HUVEC cells.

Effect of flupirtine on cell death of human umbilical vein endothelial cells induced by reactive oxygen species

1998 ◽  
Vol 56 (12) ◽  
pp. 1615-1624 ◽  
Author(s):  
Bernd Lorenz ◽  
Thomas Schlüter ◽  
Ralf Bohnensack ◽  
Gabriela Pergande ◽  
Werner E.G Müller
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Cell Death ◽  
Umbilical Vein ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals Verocytotoxin-Induced Apoptosis of Human Microvascular Endothelial Cells

2001 ◽  
Vol 12 (4) ◽  
pp. 767-778
Author(s):  
ANTONETTA H. J. M. PIJPERS ◽  
PETRA A. VAN SETTEN ◽  
LAMBERTUS P. W. J. VAN DEN HEUVEL ◽  
KAREL J. M. ASSMANN ◽  
HENDRIKUS B. P. M. DIJKMAN ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Protein Synthesis ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Microvascular Endothelial Cells ◽  
Tnf Α ◽  
Microvascular Endothelial ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

Abstract. The pathogenesis of the epidemic form of hemolytic uremic syndrome is characterized by endothelial cell damage. In this study, the role of apoptosis in verocytotoxin (VT)-mediated endothelial cell death in human glomerular microvascular endothelial cells (GMVEC), human umbilical vein endothelial cells, and foreskin microvascular endothelial cells (FMVEC) was investigated. VT induced apoptosis in GMVEC and human umbilical vein endothelial cells when the cells were prestimulated with the inflammatory mediator tumor necrosis factor-α (TNF-α). FMVEC displayed strong binding of VT and high susceptibility to VT under basal conditions, which made them suitable for the study of VT-induced apoptosis without TNF-α interference. On the basis of functional (flow cytometry and immunofluorescence microscopy using FITC-conjugated annexin V and propidium iodide), morphologic (transmission electron microscopy), and molecular (agarose gel electrophoresis of cellular DNA fragments) criteria, it was documented that VT induced programmed cell death in microvascular endothelial cells in a dose- and time-dependent manner. Furthermore, whereas partial inhibition of protein synthesis by VT was associated with a considerable number of apoptotic cells, comparable inhibition of protein synthesis by cycloheximide was not. This suggests that additional pathways, independent of protein synthesis inhibition, may be involved in VT-mediated apoptosis in microvascular endothelial cells. Specific inhibition of caspases by Ac-Asp-Glu-Val-Asp-CHO, but not by Ac-Tyr-Val-Ala-Asp-CHO, was accompanied by inhibition of VT-induced apoptosis in FMVEC and TNF-α-treated GMVEC. These data indicate that VT can induce apoptosis in human microvascular endothelial cells.

431 GENERATION OF CLONED CD55-CD39 TRANSGENIC α1,3-GALACTOSYLTRANSFERASE DEPLETED (GAL - / - ) PIGLETS

2010 ◽  
Vol 22 (1) ◽  
pp. 372
Author(s):  
A. Perota ◽  
D. Brunetti ◽  
B. Charreau ◽  
M. Chatelais ◽  
I. Lagutina ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Nuclear Transfer ◽  
Umbilical Vein ◽  
Expression Level ◽  
Expression Vectors ◽  
Rt Pcr ◽  
Complete Evaluation ◽  
Huvec Cells ◽  
Umbilical Vein Endothelial Cells ◽  
High Level

Success in xenotransplantation relies on engineering of the pig genome to express human transgenes, such as CD55/CD39, that can control coagulation and inflammation to prolong the graft survival of a 1,3-galactosyltransferase depleted (Gal-/-) pig organs in nonhuman primates and then able to bypass the hyperacute rejection. The aim of our work was to produce Gal-/- piglets overexpressing CD55/CD39. In experiment (Exp.) 1 exploiting 2 ubiquitous expression vectors (pCAGGS-CD55 and pCAGGS-CD39), we transfected immortalized porcine kidney cells (PK15) with CD55 and CD39 using Nucleofector (Amaxa Biosystems, Cologne, Germany) and selected 5 cell colonies each (PK15-CD55 and PK15-CD39) that were expanded and analyzed by RT-PCR, immunohistochemistry (IHC) and Western blot (WB). The monoclonal antibodies IA10 for hCD55 and BU61 for hCD39 were used. Transgenic transcription was confirmed by Northern blot (NB) using digoxigenin-labeled probes. In Exp. 2, a neonatal pig Gal-/- fibroblast line was co-transfected by Nucleofector using 2 ubiquitous expression vectors (hEF-CD55 and pCAGGS-CD39) for the expression of CD55 and CD39. Colonies were analyzed by RT-PCR and IHC only, because of the limited number of cells available. Cells from one colony with a high level of CD55/CD39 expression according to IHC were used for nuclear transfer into enucleated oocytes. Day 5 compact morula/blastocyst (n = 144) were transplanted in 2 synchronized sows. Porcine aortic endothelial cells (PAEC) and fibroblasts derived from 2 stillborn piglets were analysed with IHC, NB, and WB. The expression level of transgenes from both experiments was compared with human umbilical vein endothelial cells (HUVEC) by fluorescence-activated cell sorting (FACS), using IA10, BRIC110, IH4, 2G2, and MEM-118 antibodies for hCD55 and TU66 for hCD39. In Exp. 1, RT-PCR showed CD55 mRNA expression in 3 out of 5 (2, 15, 24) PK15-CD55 colonies. A high level of CD55 expression was confirmed only in colony 24 by IHC, NB, WB, and FACS. Low expression level in colony 2 revealed by FACS was not detected by IHC, indicating that FACS analysis is more accurate to quantify the level of expression. All PK15-CD39 colonies were positive according to RT-PCR and IHC. Only one colony PK15-CD39 was further analyzed by NB and WB and confirmed positive. In Exp. 2, IHC, NB, WB, and FACS analyses of fibroblasts and PAEC derived from both cloned piglets confirmed the high level of CD39 expression detected by IHC in donor cells used for nuclear transfer. However, strong CD55 expression detected by IHC was not confirmed by NB analyses and, by FACS, was lower than in HUVEC cells. In conclusion, we produced cloned CD55-CD39 transgenic Gal-/- piglets with a high level of CD39 expression but the expression level of CD55 was lower than in HUVEC cells. We found that although IHC is the method of choice in preliminary screening, it is not sufficiently quantitative when only a few cells for each clone are available. Thus, IHC needs to be complemented with additional methods (e.g. WB, FACS, real-time RT-PCR) to obtain complete evaluation of the expression pattern of transgenes before nuclear transfer experiments. This study was supported by EU grant no. LSHB-CT-2006-037377 and Fondazione Banca Popolare di Cremona.

Vitamin D decreases cell death and inflammation in human umbilical vein endothelial cells and placental explants from pregnant women with preeclampsia cultured with TNF-α

2021 ◽  
pp. 1-17
Author(s):  
Priscila Rezeck Nunes ◽  
Mariana Romao-Veiga ◽  
Vanessa Rocha Ribeiro ◽  
Larissa Ragozo Cardoso de Oliveira ◽  
Thiago Gameiro Zupelli ◽  
...  
Keyword(s):  
Vitamin D ◽  
Endothelial Cells ◽  
Cell Death ◽  
Pregnant Women ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells
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