scholarly journals Vascular and Blood Compatibility of Engineered Cationic Cellulose Nanocrystals in Cell-Based Assays

Nanomaterials ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2072
Author(s):  
Alexandre Bernier ◽  
Tanner Tobias ◽  
Hoang Nguyen ◽  
Shreshth Kumar ◽  
Beza Tuga ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Viability ◽  
Cellulose Nanocrystals ◽  
Blood Compatibility ◽  
Biological Activities ◽  
Umbilical Vein ◽  
Circulatory System ◽  
Dependent Manner ◽  
Umbilical Vein Endothelial Cells ◽  
The Impact

An emerging interest regarding nanoparticles (NPs) concerns their potential immunomodulatory and pro-inflammatory activities, as well as their impact in the circulatory system. These biological activities of NPs can be related to the intensity and type of the responses, which can raise concerns about adverse side effects and limit the biomedical applicability of these nanomaterials. Therefore, the purpose of this study was to investigate the impact of a library of cationic cellulose nanocrystals (CNCs) in the human blood and endothelial cells using cell-based assays. First, we evaluated whether the cationic CNCs would cause hemolysis and aggregation or alteration on the morphology of red blood cells (RBC). We observed that although these nanomaterials did not alter RBC morphology or cause aggregation, at 24 h exposure, a mild hemolysis was detected mainly with unmodified CNCs. Then, we analyzed the effect of various concentrations of CNCs on the cell viability of human umbilical vein endothelial cells (HUVECs) in a time-dependent manner. None of the cationic CNCs caused a dose-response decrease in the cell viability of HUVEC at 24 h or 48 h of exposure. The findings of this study, together with the immunomodulatory properties of these cationic CNCs previously published, support the development of engineered cationic CNCs for biomedical applications, in particular as vaccine nanoadjuvants.

scholarly journals Homocysteine Induces Apoptosis of Human Umbilical Vein Endothelial Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Zhimin Zhang ◽  
Congying Wei ◽  
Yanfen Zhou ◽  
Tao Yan ◽  
Zhengqiang Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Umbilical Vein ◽  
Dependent Manner ◽  
Human Umbilical Vein ◽  
Homologous Protein ◽  
Intracellular Ros ◽  
Underlying Mechanisms ◽  
Umbilical Vein Endothelial Cells

Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspase-3. Prolonged Hcy treatment also upregulated glucose-regulated protein 78 (GRP78), activated protein kinase RNA-like ER kinase (PERK), and induced the expression of C/EBP homologous protein (CHOP) and the phosphorylation of NF-κb. The inhibition of NOX4 decreased the production of ROS and alleviated the Hcy-induced HUVEC apoptosis and ER stress. Blocking the PERK pathway partly alleviated Hcy-induced HUVEC apoptosis and the activation of NF-κb. Taken together, our results suggest that Hcy-induced mitochondrial dysfunction crucially modulated apoptosis and contributed to the activation of ER stress in HUVEC. The excessive activation of the PERK pathway partly contributed to Hcy-induced HUVEC apoptosis and the phosphorylation of NF-κb.

scholarly journals Citrus bergamiaRisso Elevates Intracellular Ca2+in Human Vascular Endothelial Cells due to Release of Ca2+from Primary Intracellular Stores

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Purum Kang ◽  
Seung Ho Han ◽  
Hea Kyung Moon ◽  
Jeong-Min Lee ◽  
Hyo-Keun Kim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Channel Blocker ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Concentration Dependent Manner ◽  
Carbonyl Cyanide ◽  
Intracellular Ca ◽  
Umbilical Vein Endothelial Cells

The purpose of the present study is to examine the effects of essential oil ofCitrus bergamiaRisso (bergamot, BEO) on intracellular Ca2+in human umbilical vein endothelial cells. Fura-2 fluorescence was used to examine changes in intracellular Ca2+concentration[Ca2+]i. In the presence of extracellular Ca2+, BEO increased[Ca2+]i, which was partially inhibited by a nonselective Ca2+channel blocker La3+. In Ca2+-free extracellular solutions, BEO increased[Ca2+]iin a concentration-dependent manner, suggesting that BEO mobilizes intracellular Ca2+. BEO-induced[Ca2+]iincrease was partially inhibited by a Ca2+-induced Ca2+release inhibitor dantrolene, a phospholipase C inhibitor U73122, and an inositol 1,4,5-triphosphate (IP3)-gated Ca2+channel blocker, 2-aminoethoxydiphenyl borane (2-APB). BEO also increased[Ca2+]iin the presence of carbonyl cyanide m-chlorophenylhydrazone, an inhibitor of mitochondrial Ca2+uptake. In addition, store-operated Ca2+entry (SOC) was potentiated by BEO. These results suggest that BEO mobilizes Ca2+from primary intracellular stores via Ca2+-induced and IP3-mediated Ca2+release and affect promotion of Ca2+influx, likely via an SOC mechanism.

scholarly journals Endothelial AMP-Activated Kinase α1 Phosphorylates eNOS on Thr495 and Decreases Endothelial NO Formation

2018 ◽  
Vol 19 (9) ◽  
pp. 2753 ◽  
Author(s):  
Nina Zippel ◽  
Annemarieke Loot ◽  
Heike Stingl ◽  
Voahanginirina Randriamboavonjy ◽  
Ingrid Fleming ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Reactivity ◽  
Umbilical Vein ◽  
No Production ◽  
Dependent Manner ◽  
Calmodulin Binding ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Nitric Oxide ◽  
Specific Deletion

AMP-activated protein kinase (AMPK) is frequently reported to phosphorylate Ser1177 of the endothelial nitric-oxide synthase (eNOS), and therefore, is linked with a relaxing effect. However, previous studies failed to consistently demonstrate a major role for AMPK on eNOS-dependent relaxation. As AMPK also phosphorylates eNOS on the inhibitory Thr495 site, this study aimed to determine the role of AMPKα1 and α2 subunits in the regulation of NO-mediated vascular relaxation. Vascular reactivity to phenylephrine and acetylcholine was assessed in aortic and carotid artery segments from mice with global (AMPKα−/−) or endothelial-specific deletion (AMPKαΔEC) of the AMPKα subunits. In control and AMPKα1-depleted human umbilical vein endothelial cells, eNOS phosphorylation on Ser1177 and Thr495 was assessed after AMPK activation with thiopental or ionomycin. Global deletion of the AMPKα1 or α2 subunit in mice did not affect vascular reactivity. The endothelial-specific deletion of the AMPKα1 subunit attenuated phenylephrine-mediated contraction in an eNOS- and endothelium-dependent manner. In in vitro studies, activation of AMPK did not alter the phosphorylation of eNOS on Ser1177, but increased its phosphorylation on Thr495. Depletion of AMPKα1 in cultured human endothelial cells decreased Thr495 phosphorylation without affecting Ser1177 phosphorylation. The results of this study indicate that AMPKα1 targets the inhibitory phosphorylation Thr495 site in the calmodulin-binding domain of eNOS to attenuate basal NO production and phenylephrine-induced vasoconstriction.

scholarly journals Effects of paeonol on the expression of NF-κB pathways in human umbilical veins endothelial cells induced by homocysteine

2015 ◽  
Vol 10 (3) ◽  
pp. 604
Author(s):  
Qian Xu ◽  
Kai Cao ◽  
Yan-Hong Xiao ◽  
Chao Du ◽  
Xian-Hui Dong ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Cell Viability ◽  
Protein Degradation ◽  
Mrna Expression ◽  
Umbilical Vein ◽  
Model Group ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

<p class="Abstract">The aim of this study was to investigate the effects of paeonol on the expression of NF-κB pathway induced by homocysteine. After Human umbilical vein endothelial cells exposed to homocysteine for 24 hours,  paeonol (0.15-0.6 mmol/L) improved the cell viability (p&lt;0.05). NF-κB p65 mRNA expression was reduced largely (p&lt;0.05) and IκB-α protein expression increased significantly (p&lt;0.01). The staining of NF-κB p65 in nucleus was not as much as those in homocysteine injured model group (p&lt;0.01). Therefore, paeonol can inhibit IκB-α protein degradation and suppress NF-κB transferred into nuclear in order to inhibit the activation of NF-κB.</p><p> </p>

Protease Dependent Activation of Endothelial Cells by Peritoneal Dialysis Effluents

1999 ◽  
Vol 82 (10) ◽  
pp. 1334-1341 ◽  
Author(s):  
Michael Krebs ◽  
Christoph Kaun ◽  
Matthias Lorenz ◽  
Marianne Haag-Weber ◽  
Bernd Binder ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Peritoneal Dialysis ◽  
Umbilical Vein ◽  
Procoagulant Activity ◽  
Partial Purification ◽  
Complement Factor ◽  
Dependent Manner ◽  
Facs Analysis ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

SummaryIncubation of cultured human umbilical vein endothelial cells (HUVECs) with dilutions of peritoneal dialysis effluents (PDEs) from 11 individual patients undergoing continuous ambulatory peritoneal dialysis (CAPD) induced cellular procoagulant activity in a dose and time dependent manner. This procoagulant activity could be attributed to tissue factor (TF) expression since it was blocked by rabbit anti-TF IgG. These data was confirmed by FACS analysis yielding surface TF expression; In addition PDEs induced the expression of E-selectin in HUVECs. This TF and selectin inducing activity was heat labile and could be inhibited by protease inhibitors. Partial purification could be achieved using a benzamidine-Sepharose column. The TF inducing activity could not be attributed to LPS, IL-1, TNF-α, mast cell tryptase, active thrombin, or complement factor D. We therefore conclude that the peritoneal cavity contains a protease activity that induces a procoagulatory and proinflammatory phenotype in HUVECs.

Daunorubicin induces procoagulant activity of cultured endothelial cells through phosphatidylserine exposure and microparticles release

2010 ◽  
Vol 104 (12) ◽  
pp. 1235-1241 ◽  
Author(s):  
Huibo Li ◽  
Fenglin Cao ◽  
Yanhua Su ◽  
Shengjin Fan ◽  
Yinghua Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Chemotherapeutic Agents ◽  
Significant Inhibition ◽  
Procoagulant Activity ◽  
Clotting Time ◽  
Increased Risk ◽  
Umbilical Vein Endothelial Cells ◽  
The Impact ◽  
Prothrombotic Effect

SummaryAdministration of various chemotherapeutic agents is associated with an increased risk of thrombotic events. Although vascular endothelium plays a predominant role in blood coagulation and fibrinolysis, the effect of cytotoxic drugs on the procoagulant activity (PCA) of endothelial cells has not been well evaluated. Our study aims to investigate the possibility that daunorubicin, a chemotherapeutic agent, exerts prothrombotic effect on endothelial cells. We tested the impact of daunorubicin on phosphatidylserine (PS) exposure, endothelial microparticles (EMPs) release and consequent PCA. Human umbilical vein endothelial cells (HUVECs) were treated with daunorubicin (0.1, 0.2, 0.5, 1, 2 μM) for 24 hours. PCA of HUVECs was measured using clotting time and purified coagulation complex assays. Counts and PCA of EMPs were evaluated by flow cytometry and clotting time assay, respectively. Lactadherin was used as a novel probe for detection of PS exposure and EMPs release. We found that daunorubicin dose-dependently increased the PS exposure and consequent PCA of HUVECs. Moreover, daunorubicin treatment also enhanced the release of EMPs which were highly procoagulant. This increment was especially significant at 0.2 μM of daunorubicin or more. Blockade of PS with lactadherin inhibited over 90% of HUVECs and EMPs PCA. However, anti-TF antibody had no significant inhibition effect. Our results demonstrate that daunorubicin treatment enhanced PCA of HUVECs through PS exposure and shedding of procoagulant EMPs. Lactadherin acts as an efficient anticoagulant in this process.

scholarly journals The Induction of Cyclooxygenase-2 in IL-1β-Treated Endothelial Cells is Inhibited by Prostaglandin E2 through cAMP

1999 ◽  
Vol 8 (6) ◽  
pp. 287-294 ◽  
Author(s):  
Pravit Akarasereenont ◽  
Kitirat Techatrisak ◽  
Sirikul Chotewuttakorn ◽  
Athiwat Thaworn
Keyword(s):  
Endothelial Cells ◽  
Biological Activities ◽  
Umbilical Vein ◽  
The Body ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Negative Feedback Regulation ◽  
Cox 2 ◽  
Arachidonic Acids ◽  
Cox 1

Prostaglandins (PGS) have numerous cardiovascular and inflammatory effects. Cyclooxygenase (COX), which exists as COX-1 and COX-2 isoforms, is the first enzyme in the pathway in which arachidonic acid is converted to PGs. Prostaglandin E2 (PGE2) exerts a variety of biological activities for the maintenance of local homeostasis in the body. Elucidation of PGE2 involvement in the signalling molecules such as COX could lead to potential therapeutic interventions. Here, we have investigated the effects of PGE2 on the induction of COX-2 in human umbilical vein endothelial cells (HUVEC) treated with interleukin-1β (IL-1β 1 ng/ml). COX activity was measured by the production of 6-keto-PGF1α, PGE2, PGF2α and thromboxane B2 (TXB2) in the presence of exogenous arachidonic acids (10 μM for 10 min) using enzyme immunoassay (EIA). COX-1 and COX-2 protein was measured by immunoblotting using specific antibody. Untreated HUVEC contained only COX-1 protein while IL-1β treated HUVEC contained COX-1 and COX-2 protein. PGE2 (3 μM for 24 h) did not affect on COX activity and protein in untreated HUVEC. Interestingly, PGE2 (3 μM for 24 h) can inhibit COX-2 protein, but not COX-1 protein, expressed in HUVEC treated with IL1 β. This inhibition was reversed by coincubation with forskolin (100 μM). The increased COX activity in HUVEC treated with IL-1β was also inhibited by PGE2 (0.03, 0.3 and 3 μM for 24 h) in a dose-dependent manner. Similarly, forskolin (10, 50 or 100 μM) can also reverse the inhibition of PGE2 on increased COX activity in IL-1β treated HUVEC. The results suggested that (i) PGE2 can initiate negative feedback regulation in the induction of COX-2 elicited by IL-1β in endothelial cells, (ii) the inhibition of PGE2 on COX-2 protein and activity in IL-1β treated HUVEC is mediated by cAMP and (iii) the therapeutic use of PGE2 in the condition which COX-2 has been involved may have different roles.

The Platelet Specific Chemokine Platelet Factor 4 Induces Expression of E-Selectin in an NF-κ B Dependent Manner.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3908-3908
Author(s):  
Bruce S. Sachais ◽  
Peihong Ma ◽  
Ann H. Rux ◽  
Guangyao Yu
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Atherosclerotic Lesion ◽  
Surface Expression ◽  
Platelet Factor 4 ◽  
Dependent Manner ◽  
Mobility Shift ◽  
Platelet Factor ◽  
Umbilical Vein Endothelial Cells ◽  
Electrophoretic Mobility Shift Assays

Abstract The involvement of platelets in the pathogenesis of atherosclerosis has recently gained much attention. Platelet factor 4 (PF4) is a platelet specific chemokine released upon platelet activation. PF4 has been localized to atherosclerotic lesions, including macrophages and endothelium. In this report, we demonstrate that E-selectin, an adhesion molecule involved in atherogenesis, is up-regulated in human umbilical vein endothelial cells exposed to PF4. Induction of E-selectin mRNA is time and dose dependent, and requires the presence of cell surface glycosaminoglycans. Surface expression of E-selectin, as measured by flow cytometry, is also increased by PF4. Activation of NF-κB is critical for PF4 induced E-selectin expression, as demonstrated by promoter activation studies and electrophoretic mobility shift assays. In summary, our data demonstrate that PF4 can increase expression of E-selectin by endothelial cells by activation of NF-κB. PF4 induction of endothelial E-selectin expression represents another mechanism by which platelets may participate in atherosclerotic lesion progression. These data also suggest that PF4 may participate in the proinflammatory functions of activated platelets.

Daunorubicin Induces Procoagulant Activity of Cultured Endothelial Cells through Phosphatidylserine Exposure and Microparticles Release

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 5185-5185
Author(s):  
Yueyue Fu ◽  
Huibo Li ◽  
Wen Li ◽  
Xiushuai Dong ◽  
Jinxiao Hou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Conflicts Of Interest ◽  
Umbilical Vein ◽  
Chemotherapeutic Agents ◽  
Significant Inhibition ◽  
Procoagulant Activity ◽  
Clotting Time ◽  
Increased Risk ◽  
Umbilical Vein Endothelial Cells ◽  
The Impact

Abstract Abstract 5185 Administration of various chemotherapeutic agents is associated with an increased risk of thrombotic events. Although vascular endothelium plays a predominant role in blood coagulation and fibrinolysis, the effect of cytotoxic drugs on the procoagulant activity (PCA) of endothelial cells has not been well evaluated. Our study aims to investigate the possibility that daunorubicin, a chemotherapeutic agent, exerts prothrombotic effect on endothelial cells. We tested the impact of daunorubicin on phosphatidylserine (PS) exposure, endothelial microparticles (EMPs) release and consequent PCA. Human umbilical vein endothelial cells (HUVECs) were treated with daunorubicin (0.1, 0.2, 0.5, 1, 2 μ M) for 24 h. PCA of HUVECs was measured using clotting time and purified coagulation complex assays. Counts and PCA of EMPs were evaluated by flow cytometry and clotting time assay, respectively. Lactadherin was used as a novel probe for detection of PS exposure and EMPs release. We found that daunorubicin dose-dependently increased the PS exposure and consequent PCA of HUVECs. Moreover, daunorubicin treatment also enhanced the release of EMPs which were highly procoagulant. This increment was especially significant at 0.2 μ M of daunorubicin or over. Blockade of PS with lactadherin inhibited over 90% of HUVECs and EMPs PCA. However, anti-TF antibody had no significant inhibition effect. Our results demonstrate that daunorubicin treatment enhanced PCA of HUVECs through PS exposure and shedding of procoagulant EMPs. Lactadherin acts as an efficient anticoagulant in this process. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Panax Quinquefolius Saponin of Stem and Leaf Attenuates Intermittent High Glucose-Induced Oxidative Stress Injury in Cultured Human Umbilical Vein Endothelial Cells via PI3K/Akt/GSK-3βPathway

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Jingshang Wang ◽  
Huijun Yin ◽  
Ye Huang ◽  
Chunyu Guo ◽  
Chengdong Xia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Oxidative Damage ◽  
Cell Viability ◽  
High Glucose ◽  
Umbilical Vein ◽  
Panax Quinquefolius ◽  
Stress Injury ◽  
Intermittent High Glucose ◽  
Umbilical Vein Endothelial Cells

Panax quinquefolius saponin of stem and leaf (PQS), the effective parts of American ginseng, is widely used in China as a folk medicine for diabetes and cardiovascular diseases treatment. In our previous studies, we have demonstrated that PQS could improve the endothelial function of type II diabetes mellitus (T2DM) rats with high glucose fluctuation. In the present study, we investigated the protective effects of PQS against intermittent high glucose-induced oxidative damage on human umbilical vein endothelial cells (HUVECs) and the role of phosphatidylinositol 3-kinase kinase (PI3K)/Akt/GSK-3βpathway involved. Our results suggested that exposure of HUVECs to a high glucose concentration for 8 days showed a great decrease in cell viability accompanied by marked MDA content increase and SOD activity decrease. Moreover, high glucose significantly reduced the phosphorylation of Akt and GSK-3β. More importantly, these effects were even more evident in intermittent high glucose condition. PQS treatment significantly attenuated intermittent high glucose-induced oxidative damage on HUVECs and meanwhile increased cell viability and phosphorylation of Akt and GSK-3βof HUVECs. Interestingly, all these reverse effects of PQS on intermittent high glucose-cultured HUVECs were inhibited by PI3K inhibitor LY294002. These findings suggest that PQS attenuates intermittent-high-glucose-induced oxidative stress injury in HUVECs by PI3K/Akt/GSK-3βpathway.

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