scholarly journals S-Allyl-L-Cysteine Sulfoxide Inhibits Tumor Necrosis Factor-Alpha Induced Monocyte Adhesion and Intercellular Cell Adhesion Molecule-1 Expression in Human Umbilical Vein Endothelial Cells

2010 ◽  
Vol 293 (3) ◽  
pp. 421-430 ◽  
Author(s):  
Chai Hui ◽  
Wo Like ◽  
Fu Yan ◽  
Xie Tian ◽  
Wang Qiuyan ◽  
...  
Keyword(s):  
Cell Adhesion Molecule ◽  
Umbilical Vein ◽  
Monocyte Adhesion ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1 ◽  
Intercellular Cell Adhesion Molecule ◽  
Cysteine Sulfoxide ◽  
Necrosis Factor

Midazolam Inhibits Tumor Necrosis Factor-α–induced Endothelial Activation

2009 ◽  
Vol 110 (1) ◽  
pp. 106-112 ◽  
Author(s):  
Hee Kyoung Joo ◽  
Sae Cheol Oh ◽  
Eun Jung Cho ◽  
Kyoung Sook Park ◽  
Ji Young Lee ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis ◽  
Cell Adhesion Molecule ◽  
Umbilical Vein ◽  
Endothelial Activation ◽  
Monocyte Adhesion ◽  
Vascular Cell Adhesion ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1 ◽  
Necrosis Factor

Background Midazolam is widely used as an intravenous sedative. However, the role of midazolam on vascular endothelial activation is still unknown. The present study explores the action of midazolam on endothelial activation and its role to peripheral benzodiazepine receptor (PBR) in cultured human umbilical vein endothelial cells. Methods Intracellular localization of PBR in human umbilical vein endothelial cells was visualized with immunofluorescent staining. Monocyte adhesion and vascular cell adhesion molecule-1 expression were measured with monocyte adhesion assay and Western blot analysis. Involvement of PBR was assessed by using specific antagonists and small interfering RNA against PBR. Results PBR was localized in the mitochondria of human umbilical vein endothelial cells. Midazolam significantly inhibited tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 and monocyte adhesion in a dose-dependent manner (1-30 microM). The midazolam-mediated suppression on the tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 expression and monocyte adhesion were inhibited by the pretreatment of PK11195 and not inhibited by the flumazenil. Transfection of small interfering RNA for PBR decreased the expression of PBR (18 kDa) in human umbilical vein endothelial cells. Midazolam-mediated suppression on the tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 expression was abrogated by the transfection of small interfering RNA for PBR. Conclusion These results suggest that midazolam has an inhibitory action on the endothelial activation and that its action is related to the activation of peripheral benzodiazepine receptor localized in mitochondria of the endothelial cells.

scholarly journals LINC00341 exerts an anti-inflammatory effect on endothelial cells by repressing VCAM1

2017 ◽  
Vol 49 (7) ◽  
pp. 339-345 ◽  
Author(s):  
Tse-Shun Huang ◽  
Kuei-Chun Wang ◽  
Sara Quon ◽  
Phu Nguyen ◽  
Ting-Yu Chang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Rna Seq ◽  
Necrosis Factor Alpha ◽  
Polycomb Repressive Complex 2 ◽  
Health And Disease ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1

The long noncoding RNAs (lncRNAs), which constitute a large portion of the transcriptome, have gained intense research interest because of their roles in regulating physiological and pathophysiological functions in the cell. We identified from RNA-Seq profiling a set of lncRNAs in cultured human umbilical vein endothelial cells (HUVECs) that are differentially regulated by atheroprotective vs. atheroprone shear flows. Among the comprehensively annotated lncRNAs, including both known and novel transcripts, LINC00341 is one of the most abundant lncRNAs in endothelial cells. Moreover, its expression level is enhanced by atheroprotective pulsatile shear flow and atorvastatin. Overexpression of LINC00341 suppresses the expression of vascular cell adhesion molecule 1 (VCAM1) and the adhesion of monocytes induced by atheroprone flow and tumor necrosis factor-alpha. Underlying this anti-inflammatory role, LINC00341 guides enhancer of zest homolog 2, a core histone methyltransferase of polycomb repressive complex 2, to the promoter region of the VCAM1 gene to suppress VCAM1. Network analysis reveals that the key signaling pathways (e.g., Rho and PI3K/AKT) are co-regulated with LINC00341 in endothelial cells in response to pulsatile shear. Together, these findings suggest that LINC00341, as an example of lncRNAs, plays important roles in modulating endothelial function in health and disease.

Proteasome from cytokine-treated human cells shows stimulated BrAAP activity and depressed PGPH activity

2000 ◽  
Vol 78 (2) ◽  
pp. 115-118 ◽  
Author(s):  
Judith E Nelson ◽  
Claudia Altschuller-Felberg ◽  
Anna Loukissa ◽  
Christopher Cardozo
Keyword(s):  
Interferon Gamma ◽  
Umbilical Vein ◽  
Necrosis Factor Alpha ◽  
Multicatalytic Proteinase ◽  
Branched Chain Amino Acid ◽  
Factor Alpha ◽  
Branched Chain ◽  
Umbilical Vein Endothelial Cells ◽  
Multicatalytic Proteinase Complex ◽  
Necrosis Factor

The branched chain amino acid-preferring (BrAAP) activity of multicatalytic proteinase complex isolated from human umbilical vein endothelial cells and treated with interferon-gamma was increased more than 2-fold, which was associated with a marked increase in LMP7 expression and decreased peptidylglutamyl peptide-hydrolyzing activity. Increases in BrAAP activity in supernatants from cells treated with interferon-gamma, tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, or lipopolysaccharide paralleled the increases in LMP7 expression. These findings are consistent with the conclusion that the increased BrAAP activity of LMP-containing multicatalytic proteinase complex results from incorporation of LMP7 or other LMP subunits.

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