scholarly journals Endothelium and Its Alterations in Cardiovascular Diseases: Life Style Intervention

2014 ◽  
Vol 2014 ◽  
pp. 1-28 ◽  
Author(s):  
Gaia Favero ◽  
Corrado Paganelli ◽  
Barbara Buffoli ◽  
Luigi Fabrizio Rodella ◽  
Rita Rezzani
Keyword(s):  
Endothelial Cell ◽  
Cardiovascular Diseases ◽  
Cell Activation ◽  
Cell Function ◽  
Leukocyte Adhesion ◽  
Endothelial Cell Activation ◽  
Endothelial Cell Function ◽  
Beneficial Effects ◽  
Life Style Intervention ◽  
Endothelial Functions

The endothelium, which forms the inner cellular lining of blood vessels and lymphatics, is a highly metabolically active organ that is involved in many physiopathological processes, including the control of vasomotor tone, barrier function, leukocyte adhesion, and trafficking and inflammation. In this review, we summarized and described the following: (i) endothelial cell function in physiological conditions and (ii) endothelial cell activation and dysfunction in the main cardiovascular diseases (such as atherosclerosis, and hypertension) and to diabetes, cigarette smoking, and aging physiological process. Finally, we presented the currently available evidence that supports the beneficial effects of physical activity and various dietary compounds on endothelial functions.

Modulation of Endothelial Cell Function by Antiphospholipid Antibodies

Lupus ◽  
1996 ◽  
Vol 5 (5) ◽  
pp. 448-450 ◽  
Author(s):  
PL Meroni ◽  
N Del Papa ◽  
B Beltrami ◽  
A Tincani ◽  
G Balestrieri ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Activation ◽  
Cell Function ◽  
Arachidonic Acid Metabolism ◽  
Endothelial Cell Activation ◽  
Endothelial Cell Function ◽  
Cofactor Binding ◽  
Cell Functions ◽  
Glycoprotein I ◽  
Gamma Irradiated

β2-glycoprotein I (β2-GP-I) the plasma cofactor for anti-phospholipid antibodies adheres on the endothelial surfaces and can be recognized by anti-β2-GP-I antibodies naturally occurring in patients with the anti-phospholipid syndrome. As for the cofactor binding to cardiolipin- or gamma irradiated-plates, the endothelial binding is mediated by the so-called phospholipid binding site, a cationic structure able to react with anionic molecules. Endothelial monolayers appear to represent a substrate able to bind β2-GP-I and to present it in a suitable manner in order to allow the binding of anti-β2-GP-I β2 antibodies. The complex between β2-GP-I and the respective antibodies induce an endothelial cell activation as demonstrated by the up-regulation of adhesion molecule expression, the secretion of proinflammatory cytokines and the modulation of arachidonic acid metabolism. Taken together these findings strongly sustain a pivotal role for β2-GP-I in allowing antibody deposition on the endothelium and in affecting endothelial cell functions potentially responsible for a procoagulant state.

6-Methylsulfinylhexyl isothiocyanate modulates endothelial cell function and suppresses leukocyte adhesion

2013 ◽  
Vol 68 (1) ◽  
pp. 144-153 ◽  
Author(s):  
Takayuki Okamoto ◽  
Nobuyuki Akita ◽  
Masashi Nagai ◽  
Tatsuya Hayashi ◽  
Koji Suzuki
Keyword(s):  
Endothelial Cell ◽  
Cell Function ◽  
Leukocyte Adhesion ◽  
Endothelial Cell Function

scholarly journals Xenogeneic Serum Promotes Leukocyte-Endothelium Interaction under Flow through Two Temporally Distinct Pathways

1999 ◽  
Vol 10 (10) ◽  
pp. 2197-2207
Author(s):  
MARINA MORIGI ◽  
CARLA ZOJA ◽  
STELLA COLLEONI ◽  
STEFANIA ANGIOLETTI ◽  
BARBARA IMBERTI ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Human Serum ◽  
Cell Activation ◽  
Leukocyte Adhesion ◽  
Endothelial Cell Activation ◽  
Porcine Serum ◽  
Confocal Fluorescence ◽  
Adhesive Molecules ◽  
H 30

Abstract. Endothelial cell activation and mononuclear cell infiltration are consistent features of discordant xenograft rejection. This study evaluated whether xenogeneic serum—as a source of xenoreactive natural antibodies and complement—induced endothelial activation with consequent leukocyte adhesion and transmigration under flow conditions. Porcine aortic endothelial cells (PAEC) were incubated for 30 min, 1 h 30 min, or 5 h with 10% human serum or 10% porcine serum and then perfused with human leukocytes in a parallel plate flow chamber under flow (1.5 dynes/cm2). Adherent and transmigrated cells were counted by digital image analysis. Results showed that human serum significantly (P < 0.01) increased over time the number of adherent leukocytes compared with porcine serum. Stimulation of PAEC with human serum also promoted a progressive increase in leukocyte transmigration that reached statistical significance (P < 0.01) at 1 h 30 min and at 5 h compared with porcine serum. Studying the role of complement in leukocyte-endothelium interaction in xenogeneic conditions, a marked complement C3 deposition on PAEC exposed to human serum was shown by immunofluorescence, whereas cells incubated with procine serum were negative. Next, it was documented that human serum decomplemented by heating and C3-deficient human serum failed to promote both leukocyte adhesion and transmigration, results that were comparable to porcine serum. To elucidate the intracellular mediators involved in endothelial cell activation by xenogeneic serum, this study focused on transcriptional factor nuclear factor-κB (NF-κB), a central regulator for the induction of different genes, including adhesive molecules and chemoatractants. Positive nuclear staining of NF-κB (p65 subunit) found by confocal fluorescence microscopy of PAEC exposed to human serum was taken to reflect NF-κB activation. NF-κB was instead strictly localized in the cell cytoplasm in PAEC incubated with the homologous serum. Heat-inactivated human serum failed to activate NF-κB. Electrophoretic mobility shift assay of nuclear extracts from PAEC exposed to human serum revealed an intense NF-κB activation that was inhibited by the NF-κB inhibitor pyrrolidinedithiocarbamate. The NF-κB inhibitors pyrrolidinedithiocarbamate and tosyl-phe-chloromethylketone did not affect the number of adherent and transmigrated leukocytes in PAEC exposed to human serum for 30 min and 1 h 30 min. Both inhibitors instead significantly reduced leukocyte adhesion and transmigration induced by human serum at 5 h. Confocal fluorescence microscopy studies showed that human serum induced an increase in the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. Functional blocking of these adhesive molecules with the corresponding antibodies significantly inhibited xenogeneic serum-induced leukocyte adhesion. These data suggest that leukocyte adhesion and transmigration are directly dependent on complement deposited on PAEC in the early phase of cell activation (30 min and 1 h 30 min) induced by xenogeneic serum, whereas leukocyte adhesive events observed after 5 h of incubation of endothelial cells with xenogeneic serum are possibly regulated by transcription of NF-κB-dependent genes. The finding that xenogeneic serum promotes leukocyte-endothelial interaction depending on NF-κB activation might be relevant for designing future therapeutic strategies intended to prolong xenograft survival.

Circulating Endothelial Cell/Leukocyte Adhesion Molecules in Atherosclerosis

1994 ◽  
Vol 72 (01) ◽  
pp. 151-154 ◽  
Author(s):  
Andrew D Blann ◽  
Charles N McCollum
Keyword(s):  
Endothelial Cell ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Leukocyte Adhesion ◽  
Clinical Manifestations ◽  
Intercellular Adhesion Molecule ◽  
Endothelial Cell Activation ◽  
Soluble Adhesion Molecules ◽  
Von Willebrand

SummarySoluble adhesion molecules E-selectin, intercellular adhesion molecule (sICAM) and vascular cell adhesion molecule (sVCAM) were measured alongside von Willebrand factor (vWf) in 40 patients with peripheral vascular disease (PVD), 43 with ischaemic heart disease (IHD) and in equal numbers of age and sex matched asymptomatic controls. Increased vWf was found in patients with IHD (p = 0.0008) and in patients with PVD (p = 0.0001) relative to their respective controls but levels did not differ between the two patient groups. Raised sICAM was found in both PVD (p = 0.0003) and IHD (p = 0.0059) compared to their respective controls and was higher in PVD than in IHD (p = 0.0088). In the subjects taken as a whole, there was no correlation between vWf and sICAM. Levels of soluble E-sel-ectin and sVCAM did not differ in patients or controls. These data suggest that soluble ICAM may be useful as an index of endothelial cell activation in clinical manifestations of atherosclerosis.

scholarly journals Enhancing Antitumor Efficacy of Heavily Vascularized Tumors by RAMBO Virus through Decreased Tumor Endothelial Cell Activation

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1040
Author(s):  
Mitra Nair ◽  
Maninder Khosla ◽  
Yoshihiro Otani ◽  
Margaret Yeh ◽  
Flora Park ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Solid Tumors ◽  
Cell Activation ◽  
Leukocyte Adhesion ◽  
Oncolytic Viruses ◽  
Endothelial Cell Activation ◽  
Microscopy Imaging ◽  
Activation Markers

Vascularization is a common pathology for many solid tumors, and therefore anti-angiogenic strategies are being investigated as a therapeutic target for treatment. Numerous studies are also being conducted regarding the effects of oncolytic viruses, including ImlygicTM, an FDA approved oncolytic herpes simplex virus-1 (oHSV) for the treatment of highly vascularized tumors such as Kaposi sarcoma (NCT04065152), and brain tumors. To our knowledge, the effects of combining oncolytic HSV with angiogenesis inhibition on endothelial cell activation has not been previously described. Here, we tested the effects of Rapid Antiangiogenesis Mediated By Oncolytic Virus (RAMBO), an oHSV which expresses a potent anti-angiogenic gene Vasculostatin on endothelial cell activation in heavily vascularized solid tumors. oHSV treatment induces endothelial cell activation, which inhibits virus propagation and oncolysis in adjacent tumor cells in vitro. Consistently, this was also observed in intravital imaging of intracranial tumor-bearing mice in vivo where infected tumor endothelial cells could efficiently clear the virus without cell lysis. Quantitative real-time PCR (Q-PCR), leukocyte adhesion assay, and fluorescent microscopy imaging data, however, revealed that RAMBO virus significantly decreased expression of endothelial cell activation markers and leukocyte adhesion, which in turn increased virus replication and cytotoxicity in endothelial cells. In vivo RAMBO treatment of subcutaneously implanted sarcoma tumors significantly reduced tumor growth in mice bearing sarcoma compared to rHSVQ. In addition, histological analysis of RAMBO-treated tumor tissues revealed large areas of necrosis and a statistically significant reduction in microvessel density (MVD). This study provides strong preclinical evidence of the therapeutic benefit for the use of RAMBO virus as a treatment option for highly vascularized tumors.

Glucose and Insulin Modulate the Capacity of Endothelial Cells (HUVEC) to Express P-selectin and Bind a Monocytic Cell Line (U937)

2001 ◽  
Vol 86 (08) ◽  
pp. 680-685 ◽  
Author(s):  
Kamal Chettab ◽  
Jacques Duhault ◽  
Elisabeth Koenig-Berard ◽  
John McGregor ◽  
Marta Puente Navazo
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Line ◽  
High Glucose ◽  
Cell Function ◽  
Leukocyte Adhesion ◽  
Human Umbilical Cord ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Endothelial Cell Function

SummaryDiabetes mellitus is associated with increased prevalence of endothelial cell dysfunction and vascular diseases. Mechanisms leading to alterations in endothelial cell function are poorly understood. We report here that hyperglycaemia results in the expression of endothelial adhesion molecules involved in leukocyte adhesion and extravasation. Incubation of human umbilical cord endothelial cells (HUVEC) with 25 mM glucose induced the expression of P-selectin. This effect was reversed by the addition of 1 nM insulin. Moreover, increased ICAM-1 expression was observed upon HUVEC incubation with 25 mM glucose. Increased adhesion of U937 cells (a monocytic cell line) to endothelial cells cultured with 25 mM glucose was observed. High glucose-induced monocytes cell adhesion was inhibited by an anti-P-selectin monoclonal antibody (LYP20). These results show that high glucose concentration activates endothelial cells leading to monocytes adhesion providing further evidence that hyperglycaemia might be implicated in vessel wall lesions contributing to diabetic vascular disease.Present address: Dr. M. D. Puente Navazo, Centre Pluridisciplinaire d’Oncologie, ISREC, Epalinges, Switzerland

ATP-MgCl2 restores depressed endothelial cell function after hemorrhagic shock and resuscitation

1995 ◽  
Vol 268 (4) ◽  
pp. H1390-H1396 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
I. H. Chaudry
Keyword(s):  
Endothelial Cell ◽  
Mesenteric Artery ◽  
Cell Function ◽  
Ringer Lactate ◽  
Endothelial Cell Function ◽  
Shed Blood ◽  
Beneficial Effects ◽  
Significant Difference ◽  
Dose Responses ◽  
Endothelium Dependent Relaxation

Although ATP-MgCl2 produces beneficial effects following various adverse circulatory conditions, it remains unknown whether this agent restores the depressed endothelial cell function [i.e., the reduced release of endothelium-derived nitric oxide (EDNO) and endothelium-derived contracting factors (EDCF)] in a model of trauma-hemorrhage and resuscitation. To determine this, rats underwent laparotomy (i.e., trauma induced), were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of shed blood volume was returned in the form of Ringer lactate (RL). The animals were then resuscitated with four times the volume of maximal bleedout with RL, following which ATP-MgCl2 (50 mumol/kg body wt) or saline was administered. At 1.5 h postresuscitation, the aorta and superior mesenteric artery (SMA) were isolated, and dose-responses for acetylcholine (ACh, an endothelium-dependent vasodilator, via EDNO) and nitroglycerin (an endothelium-independent vasodilator) were determined. In addition, hypoxia-induced contraction, a process mediated by EDCF, was assessed. The results indicate that the decreased endothelium-dependent relaxation after hemorrhage (sham 94 +/- 3 and 97 +/- 3% vs. hemorrhage 64 +/- 5 and 57 +/- 11% at 10-5 M ACh in aorta and SMA, respectively, P < 0.05) was restored with ATP-MgCl2 treatment. In contrast, there was no significant difference in nitroglycerin-induced relaxation. Moreover, the decreased hypoxia-induced aortic contraction after hemorrhage (sham 221 +/- 26 mg/ring vs. hemorrhage 124 +/- 22 mg/ring, P < 0.05) was attenuated by administration of ATP-MgCl2.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Epsins Negatively Regulate Aortic Endothelial Cell Function by Augmenting Inflammatory Signaling

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1918
Author(s):  
Yunzhou Dong ◽  
Beibei Wang ◽  
Kui Cui ◽  
Xiaofeng Cai ◽  
Sudarshan Bhattacharjee ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Activation ◽  
Adaptor Proteins ◽  
Endothelial Cell Activation ◽  
Calcium Release Channel ◽  
Inflammatory Signaling ◽  
Endothelial Cell Function ◽  
Aortic Endothelial Cells ◽  
Aortic Endothelial

Background: The endothelial epsin 1 and 2 endocytic adaptor proteins play an important role in atherosclerosis by regulating the degradation of the calcium release channel inositol 1,4,5-trisphosphate receptor type 1 (IP3R1). In this study, we sought to identify additional targets responsible for epsin-mediated atherosclerotic endothelial cell activation and inflammation in vitro and in vivo. Methods: Atherosclerotic ApoE−/− mice and ApoE−/− mice with an endothelial cell-specific deletion of epsin 1 on a global epsin 2 knock-out background (EC-iDKO/ApoE−/−), and aortic endothelial cells isolated from these mice, were used to examine inflammatory signaling in the endothelium. Results: Inflammatory signaling was significantly abrogated by both acute (tumor necrosis factor-α (TNFα) or lipopolysaccharide (LPS)) and chronic (oxidized low-density lipoprotein (oxLDL)) stimuli in EC-iDKO/ApoE−/− mice and murine aortic endothelial cells (MAECs) isolated from epsin-deficient animals when compared to ApoE−/− controls. Mechanistically, the epsin ubiquitin interacting motif (UIM) bound to Toll-like receptors (TLR) 2 and 4 to potentiate inflammatory signaling and deletion of the epsin UIM mitigated this interaction. Conclusions: The epsin endocytic adaptor proteins potentiate endothelial cell activation in acute and chronic models of atherogenesis. These studies further implicate epsins as therapeutic targets for the treatment of inflammation of the endothelium associated with atherosclerosis.

scholarly journals Inhibitory Effects of Syzygium jambos Extract on Biomarkers of Endothelial Cell Activation

2021 ◽  
Author(s):  
Yaritza Inostroza-Nieves ◽  
Shirley Valentin-Berrios ◽  
Christopher Vega ◽  
Gregory N. Prado ◽  
Claribel Luciano-Montalvo ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Cell Activation ◽  
Ex Vivo ◽  
Human Endothelial Cell ◽  
Endothelial Cell Activation ◽  
Endothelial Cell Function ◽  
Endothelial Cell Line ◽  
Syzygium Jambos ◽  
Human Endothelial Cell Line

Abstract Background: Disordered endothelial cell activation plays an important role in the pathophysiology of atherosclerosis, cancer, sepsis, viral infections, and inflammatory responses. There is interest in developing novel therapeutics to regulate endothelial cell function in atherothrombotic, metabolic, vascular, and hematological diseases. Extracts from leaves of the Syzygium jambos (L.) Alston (S. jambos) trees have been proposed to treat cardiovascular diseases and diabetes through unclear mechanisms. We investigated the effects of the S. jambos extract on biomarkers of endothelial dysfunction and immune responses in the human endothelial cell line, EA.hy926. Methods: Leaves of S. jambos were collected, concocted and lyophilized. To study the effects of S. jambos on endothelial cell activation, we used the human endothelial cell line. IL-6 levels were measured using qPCR and ELISA. PDI activity was measured using Insulin Turbidity and Di-E-GSSG assays. CM-H2DCFDA was used to study ROS levels. Migration assay was used to study S. jambos effect on ex vivo human polymorphonuclear and human mononuclear cells.Results: Our results show that incubation of EA.hy926 cells with ET-1 led to a 6.5 ± 1.6 fold increase in IL-6 expression by qPCR, an event that was blocked by S. jambos. Also, we observed that ET-1 increased extracellular protein disulfide isomerase (PDI) activity that was likewise dose-dependently blocked by S. jambos (IC50=14µg/mL). Consistent with these observations, ET-1 stimulated ex vivo human polymorphonuclear and mononuclear cell migration that also was dose-dependently blocked by S. jambos. In addition, ET-1 stimulation led to significant increases in ROS production that were sensitive to S. jambos. Conclusion: Our results suggest that the S. jambos extract represents a novel cardiovascular protective pharmacological approach to regulate endothelial cell activation, IL-6 expression, and immune-cell responses.

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