Dehydroxymethylepoxyquinomicin, a novel nuclear factor–κB inhibitor, reduces chemokines and adhesion molecule expression induced by IL-1β in human corneal fibroblasts

2014 ◽  
Vol 253 (4) ◽  
pp. 557-563 ◽  
Author(s):  
Sosuke Inokawa ◽  
Takayo Watanabe ◽  
Hiroshi Keino ◽  
Yasuhiko Sato ◽  
Akito Hirakata ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Adhesion Molecule Expression ◽  
Corneal Fibroblasts

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

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.

scholarly journals Thrombin Stimulation of the Vascular Cell Adhesion Molecule-1 Promoter in Endothelial Cells Is Mediated by Tandem Nuclear Factor-κB and GATA Motifs

2001 ◽  
Vol 276 (50) ◽  
pp. 47632-47641 ◽  
Author(s):  
Takashi Minami ◽  
William C. Aird
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Umbilical Vein ◽  
Fold Increase ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Mobility Shift ◽  
Response Element ◽  
Vascular Adhesion ◽  
Stimulation Of

The goal of this study was to delineate the transcriptional mechanisms underlying thrombin-mediated induction of vascular adhesion molecule-1 (VCAM-1). Treatment of human umbilical vein endothelial cells with thrombin resulted in a 3.3-fold increase in VCAM-1 promoter activity. The upstream promoter region of VCAM-1 contains a thrombin response element, two nuclear factor κB (NF-κB) motifs, and a tandem GATA motif. In transient transfection assays, mutation of the thrombin response element had no effect on thrombin induction. In contrast, mutation of either NF-κB site resulted in a complete loss of induction, whereas a mutation of the two GATA motifs resulted in a significant reduction in thrombin stimulation. In electrophoretic mobility shift assays, nuclear extracts from thrombin-treated endothelial cells displayed markedly increased binding to the tandem NF-κB and GATA motifs. The NF-κB complex was supershifted with anti-p65 antibodies, but not with antibodies to RelB, c-Rel, p50, or p52. The GATA complex was supershifted with antibodies to GATA-2, but not GATA-3 or GATA-6. A construct containing tandem copies of the VCAM-1 GATA motifs linked to a minimal thymidine kinase promoter was induced 2.4-fold by thrombin. Taken together, these results suggest that thrombin stimulation of VCAM-1 in endothelial cells is mediated by the coordinate action of NF-κB and GATA transcription factors.

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