scholarly journals Endothelial and Vascular Health: A Tale of Honey, H2O2 and Calcium

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1071
Author(s):  
Elia Ranzato ◽  
Gregorio Bonsignore ◽  
Mauro Patrone ◽  
Simona Martinotti
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Line ◽  
Cellular Responses ◽  
Pivotal Role ◽  
Vascular Health ◽  
Endothelial Cell Line ◽  
Positive Effects

Intracellular Ca2+ regulation plays a pivotal role in endothelial biology as well as during endothelial restoration processes. Interest in honey utilization in wound approaches is rising in recent years. In order to evaluate the positive effects of buckwheat honey on endothelial responses, we utilized an immortalized endothelial cell line to evaluate cellular responses upon honey exposure, with particular interest in Ca2+ signaling involvement. The results highlight the positive effects of buckwheat honey on endothelial cells’ responses and the central role played by Ca2+ signaling as an encouraging target for more efficacious clinical treatments.

scholarly journals Statin-induced apoptosis of vascular endothelial cells is blocked by dexamethasone

2002 ◽  
Vol 174 (1) ◽  
pp. 7-16 ◽  
Author(s):  
CJ Newton ◽  
G Ran ◽  
YX Xie ◽  
D Bilko ◽  
CH Burgoyne ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Survival ◽  
Cell Line ◽  
De Novo ◽  
Vascular Endothelial Cells ◽  
Pcr Analysis ◽  
Vascular Endothelial ◽  
Endothelial Cell Line ◽  
Induced Apoptosis

Statins block de novo synthesis of cholesterol by inhibiting the enzyme, HMG CoA reductase. The product of this reaction, mevalonic acid, is also a precursor of isoprenoids, molecules required for the activation of signalling G-proteins, such as Ras. Signal transduction pathways involving Ras are important for cell survival and this may be why statins induce apoptotic death of several cell types. Given that statins are used to treat vascular disease, it is surprising that no studies have been conducted on vascular endothelial cells. For this reason, we have tested the effect of fluvastatin (FS) on the endothelial cell line EA.hy 926. Here we show that FS, at concentrations from 1 to 2 microM, blocks growth and induces apoptosis of the endothelial cell line, EA.hy 926. As considerable redundancy exists in cell signalling pathways for cell survival, toxicity of FS under more physiological conditions might be prevented by pathways that do not require Ras, such as those activated by adrenal or sex steroids. To test this hypothesis, first RT-PCR analysis was performed for nuclear receptor mRNA expression. This revealed the presence of mRNA for the androgen receptor (AR) and glucocorticoid receptor (GR). The effect of the AR agonist, dihydrotestosterone (DHT), and the GR agonist, dexamethasone (Dex), was then tested. Whilst DHT (100 nM) had no effect on FS-induced cell death, Dex (1 microM) blocked FS-induced apoptosis. Cell cycle analysis revealed that 24 h exposure to FS prevented cells from leaving G(1) and 24-48 h later a marked sub-G(1) peak was observed. Dex was able to reduce the sub-G(1) peak, but it failed to reduce accumulation of cells in G(1). Further studies revealed that, in addition to blocking FS-induced apoptosis, Dex was able to block apoptosis of EA.hy 926 cells induced by serum deprivation, tumour necrosis factor-alpha, oxidants, DNA damage and mitochondrial disruption. This study strongly suggests that glucocorticoids have a role to play in preventing vascular injury and they may provide a reason why statins are apparently not toxic to vascular endothelial cells in vivo.

Characterization of a human endothelial cell line from a hepatic angiosarcoma

1993 ◽  
Vol 51 ◽  
pp. 14-15
Author(s):  
John M. Hoffpauir ◽  
Marie L. Hoover ◽  
Václav Větvička ◽  
Carlo H. Tamburro
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Line ◽  
Vinyl Chloride ◽  
Coagulation Factor ◽  
Human Endothelial Cell ◽  
Endothelial Cell Line ◽  
Hepatic Angiosarcoma ◽  
Human Endothelial Cell Line

Angiosarcoma of the liver is extremely rare, but there is an increased incidence in Louisville, Kentucky due to worker exposure to gaseous vinyl chloride. The tumor is endothelial in origin as it possess factor VIII, a coagulation factor and known endothelial cell marker. The malignant cells have been described as pleomorphic malignant endothelial cells, malignant spherical and spindle cells or enlarged spindle-shaped endothelial cells. The lack of a cell line derived from a hepatic angiosarcoma has significantly limited studies of this rare lethal malignancy. This study describes the characterization of a human endothelial cell line from a liver biopsy of a hepatic angiosarcoma patient who had been previously exposed to gaseous vinyl chloride. This cell line denoted, HAEND, does not require growth factors such as endothelial cell growth factor for cultivation. Also, this line can be cultivated on untreated plastic surfaces and does not require gelatin or fibronectin coated surfaces.

scholarly journals Costimulator deficient antigen presentation by an endothelial cell line induces a nonproliferative T cell activation response without anergy.

1993 ◽  
Vol 178 (5) ◽  
pp. 1597-1605 ◽  
Author(s):  
J D St Louis ◽  
J A Lederer ◽  
A H Lichtman
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
T Cell ◽  
Antigen Presentation ◽  
Cell Line ◽  
Th1 Cell ◽  
Ifn Gamma ◽  
Endothelial Cell Line ◽  
Antigen Presenting

The ability of endothelial cells to activate helper T (Th) cells by antigen presentation was studied using the murine endothelial cell line SVEC4-10 and antigen-specific murine T cell clones. SEVEC4-10 cells constitutively express vascular cell adhesion molecule 1 but not intercellular adhesion molecule 1. Interferon gamma (IFN-gamma) treatment of these cells induced class II major histocompatibility complex (MHC) expression and antigen-presenting capabilities, but did not alter surface integrin expression. IFN-gamma-treated SVEC4-10 cells were competent at mediating antigen-dependent cytokine production and proliferation of a Th2 clone. In contrast, endothelial antigen presentation to Th1 cells did not stimulate T cell proliferation. The addition of MHC mismatched spleen cells as a source of costimulatory molecules resulted in the ability of the endothelial cells to stimulate Th1 cell proliferation in an antigen-specific manner. The failure of the endothelial cell line alone to support Th1 cell proliferation correlated with the failure to stimulate interleukin 2 (IL-2) gene expression. T cell exposure to the endothelial cells plus antigen resulted in upregulation of IL-2 receptors and an enhanced response to subsequent antigen presentation by splenic antigen-presenting cells. Despite the lack of functional costimulators for IL-2 expression, antigen presentation by the endothelial cell line did not induce Th1 cell anergy, indicating that costimulator deficiency for IL-2 expression is not obligatorily linked to anergy induction. Thus, endothelial cells are capable of presenting antigens to helper T lymphocytes, but stimulate only partial T cell responses. These partial responses may serve to selectively stimulate transmigration of antigen-specific T cells and may enhance functional responses upon subsequent, extravascular antigen exposure.

A luciferase-engineered cell line for study of cAMP regulation in endothelial cells

1998 ◽  
Vol 275 (1) ◽  
pp. C75-C81 ◽  
Author(s):  
J. Xavier-Neto ◽  
A. C. Pereira ◽  
A. H. Motoyama ◽  
J. E. Krieger
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Line ◽  
Fold Increase ◽  
Positive Control ◽  
Luciferase Reporter ◽  
Luciferase Expression ◽  
Luciferase Reporter Gene ◽  
Aortic Endothelial Cells ◽  
Endothelial Cell Line

cAREL is a cAMP-responsive endothelial cell line carrying a luciferase reporter gene introduced by stable transfection of a luciferase enhancer trap into rabbit aortic endothelial cells. Luciferase gene expression in cAREL was stimulated 233-fold by 8-BrcAMP. Treatment with the β-adrenoceptor agonist isoproterenol induced a 7.0-fold increase in luciferase expression, which was partially blocked by either β1- or β2-adrenoceptor antagonists and totally blocked by propranolol and by a combination of β1- plus β2-adrenoceptor antagonists. Receptor stimulation was mimicked by cholera toxin, forskolin, 8-BrcAMP, and isobutylmethylxanthine but not by 8BrcGMP, dexamethasone, or phorbol 12-myristate 13-acetate. Stimulation by isoproterenol was completely blocked by H-89, a protein kinase A inhibitor. cAREL was also stimulated by A-23187, and this effect was abrogated by EGTA and H-89. cAREL is the first cAMP-sensitive endothelial cell line described, and it can be useful as a positive control, as a model for cAMP regulation, as a background to genetic introduction of receptors, as an indicator of intracellular pathway activation, and as a tool to investigate cAMP effects on other signaling pathways.

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