Homocysteine Inhibits TNF-α-Induced Endothelial Adhesion Molecule Expression and Monocyte Adhesion via Nuclear Factor-κB Dependent Pathway

2001 ◽  
Vol 280 (4) ◽  
pp. 1093-1100 ◽  
Author(s):  
Verena Stangl ◽  
Christoph Günther ◽  
Andres Jarrin ◽  
Peter Bramlage ◽  
Minoo Moobed ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Adhesion Molecule Expression ◽  
Monocyte Adhesion ◽  
Endothelial Adhesion Molecule ◽  
Tnf Α ◽  
Dependent Pathway

scholarly journals Inhibition of Nuclear Factor-κB–Mediated Adhesion Molecule Expression in Human Endothelial Cells

1998 ◽  
Vol 82 (3) ◽  
pp. 314-320 ◽  
Author(s):  
Jean M. Lockyer ◽  
John S. Colladay ◽  
Wendy L. Alperin-Lea ◽  
Timothy Hammond ◽  
Andrew J. Buda
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Adhesion Molecule Expression ◽  
Human Endothelial Cells

Ketamine attenuates high-glucose-mediated endothelial inflammation in human umbilical vein endothelial cells

2020 ◽  
Vol 98 (3) ◽  
pp. 156-161
Author(s):  
Tianhai Wang ◽  
Hongge Zhu ◽  
Yanshen Hou ◽  
Wenming Duan ◽  
Fufen Meng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Adhesion Molecule ◽  
High Glucose ◽  
Nuclear Translocation ◽  
Umbilical Vein ◽  
Nuclear Factor ◽  
Adhesion Molecule Expression ◽  
Endothelial Adhesion Molecule ◽  
Umbilical Vein Endothelial Cells

Hyperglycemia mediates oxidative stress, thus inducing transcription factor nuclear factor kappa B (NF-κB) activation, increasing endothelial adhesion molecule expression and monocyte/endothelial interaction, and resulting in endothelial injury. Ketamine was reported to attenuate oxidative stress in many cases. In this research, we determined whether and how ketamine protects against high-glucose-mediated augmentation of monocyte/endothelial interaction and endothelial adhesion molecule expression in human umbilical vein endothelial cells. High glucose augmented monocyte/endothelial adhesion and endothelial adhesion molecule expression. High glucose induced reactive oxygen species (ROS) production and augmented phospho-protein kinase C (p-PKC) βII expression and PKC activity. Moreover, high glucose inhibited the inhibitory subunit of nuclear factor-κBα (IκBα) expression in the cytoplasm and induced NF-κB nuclear translocation. Importantly, the effects induced by high glucose were counteracted by ketamine treatment. Further, CGP53353, a PKC βII inhibitor, inhibited high-glucose-mediated NF-κB nuclear translocation, attenuated adhesion molecule expression, and reduced monocyte/endothelial interaction. Further, these effects of ketamine against high-glucose-induced endothelial injury were inhibited by phorbol 12-myristate 13-acetate, a PKC βII activator. In conclusion, ketamine, via reducing ROS accumulation, inhibited PKC βII Ser660 phosphorylation and PKC and NF-κB activation and reduced high-glucose-induced expression of endothelial adhesion molecules and monocyte/endothelial interaction.

Differential monocyte adhesion and adhesion molecule expression in venous and arterial endothelial cells

1999 ◽  
Vol 276 (1) ◽  
pp. L9-L19 ◽  
Author(s):  
Theodore J. Kalogeris ◽  
Christopher G. Kevil ◽  
F. Stephen Laroux ◽  
Laura L. Coe ◽  
Travis J. Phifer ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Interleukin 1 ◽  
Surface Expression ◽  
Nuclear Factor Κb ◽  
Intercellular Adhesion Molecule ◽  
Nuclear Factor ◽  
Adhesion Molecule Expression ◽  
Intercellular Adhesion Molecule 1

We compared U-937 cell adhesion and adhesion molecule expression in human umbilical venous (HUVECs) and arterial (HUAECs) endothelial cells exposed to tumor necrosis factor (TNF), interleukin-1, and lipopolysaccharide (LPS). TNF and LPS stimulated vascular cell adhesion molecule (VCAM)-1 surface expression and adhesion of U-937 monocyte-like cells to HUVECs but not to HUAECs. Antibody studies demonstrated that in HUVECs at least 75% of the adhesion response is VCAM-1 mediated. Interleukin-1 stimulated U-937 cell adhesion to and VCAM-1 surface expression in both HUVECs and HUAECs. Pyrrolidinedithiocarbamate and the proteasome inhibitor MG-132 blocked TNF- and LPS-stimulated U-937 cell adhesion to HUVECs. These agents also significantly decreased TNF- and LPS-stimulated increases in HUVEC surface VCAM-1. TNF increased VCAM-1 protein and mRNA in HUVECs that was blocked by pyrrolidinedithiocarbamate. However, neither TNF or LPS stimulated VCAM-1 expression in HUAECs. TNF stimulated expression of both intercellular adhesion molecule-1 and E-selectin in HUVECs, but in HUAECs, only intercellular adhesion molecule-1 was increased. Electrophoretic mobility shift assays demonstrated no difference in the pattern of TNF-stimulated nuclear factor-κB activation between HUVECs and HUAECs. These studies demonstrate a novel and striking insensitivity of arterial endothelium to the effects of TNF and LPS and indicate a dissociation between the ability of HUAECs to upregulate nuclear factor-κB and VCAM-1.

Vascular bed origin dictates flow pattern regulation of endothelial adhesion molecule expression

2007 ◽  
Vol 292 (5) ◽  
pp. H2167-H2175 ◽  
Author(s):  
Heiko Methe ◽  
Mercedes Balcells ◽  
Maria del Carmen Alegret ◽  
Marina Santacana ◽  
Blanca Molins ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Adhesion Molecule ◽  
Immune Cell ◽  
Adhesion Molecule Expression ◽  
Endothelial Adhesion Molecule ◽  
Vascular Bed ◽  
Pathological Conditions ◽  
Coronary Artery Flow ◽  
Tnf Α ◽  
Artery Flow

Endothelial cell phenotypes markedly differ, depending upon function and vascular bed of origin. Differences might account for specific susceptibility to pathological conditions. As leukocyte adhesion to activated endothelium is the initiating event in a range of diseases, we compared the influence of vascular bed-specific flow patterns on adhesion molecule expression in human saphenous vein (HSVEC) and coronary artery endothelial cells (HCAEC). In vitro, immune cell attachment was increased 1.6-fold when tumor necrosis factor (TNF)-α-stimulated HSVEC were exposed to coronary artery flow in place of physiological venous flow and 1.9-fold higher compared with attachment to cytokine-stimulated HCAEC exposed to coronary artery flow. This was associated with increased concentrations of soluble E-selectin, VCAM-1, and ICAM-1 in supernatants of HSVEC exposed to coronary artery flow compared with HCAEC exposed to the same flow pattern. Venous and coronary artery flow both increased TNF-α-induced E-selectin and ICAM-1 expression on HSVEC, but only coronary artery flow increased VCAM-1 expression. In marked contrast to HSVEC, venous and coronary artery flow attenuated TNF-α-induced E-selectin and VCAM-1 expression on HCAEC, whereas coronary artery flow further induced ICAM-1 on cytokine-stimulated HCAEC. With the exception of cytokine-induced ICAM-1, adhesion molecule expression on HSVEC exposed to coronary artery flow exceeded expression on HCAEC. Thus ICAM-1 expression involves complex flow-dependent and -independent pathways with marked dissimilarities between the two endothelial cell types studied. Interestingly, Kruppel-like factor (KLF) 4 overexpression in HCAEC and HSVEC significantly reduced TNF-α-induced E-selectin and VCAM-1 expression in static conditions, while ICAM-1 expression remained constant. Furthermore, both flow patterns induced KLF2 and KLF4 expression in HCAEC and HSVEC. Venous and coronary artery flow differentially influence endothelial adhesion molecule and transcription factor expression, depending on the vascular bed of origin. Differences in adhesion molecule expression and subsequent immune cell adhesion between HSVEC and HCAEC may contribute to different susceptibility to pathological conditions.

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