Regular ArticleNF- κ B Independent Suppression of Endothelial Vascular Cell Adhesion Molecule-1 and Intercellular Adhesion Molecule-1 Gene Expression by Inhibition of Flavin Binding Proteins and Superoxide Production☆
References (44)
- et al.
Primary structure of ICAM-1 demonstrates interaction between members of immunoglobulin and integrin supergene families
Cell
(1988) - et al.
Human monocytes bind to two cytokine-induced adhesive ligands on cultured human endothelial cells: endothelial-leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1
Blood
(1991) - et al.
Characterization of the promoter for vascular cell adhesion molecule-1 (VCAM-1)
J Biol Chem
(1992) Lucigenin chemiluminescence in the assessment of neutrophil superoxide production
J Immunol Methods
(1987)A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding
Anal Biochem
(1976)- et al.
Cell type-specific transactivation of the VCAM-1 promoter through an NF-kappa B enhancer motif
J Biol Chem
(1995) - et al.
Vascular cell adhesion molecule-1 mediates lymphocyte adherence to cytokine-activated cultured human endothelial cells [published erratum appears in Blood 1990 Dec 1; 76(11): 2420]
Blood
(1990) - et al.
Intercellular adhesion molecule-1 gene expression in human endothelial cells: differential regulation by tumor necrosis factor- α and phorbol myristate acetate
J Biol Chem
(1992) - et al.
Activation of NF-kappa B by ER stress requires both Ca2+ and reactive oxygen intermediates as messengers
FEBS Lett
(1996) - et al.
A role for oxygen radicals as second messengers
Trends Cell Biol
(1991)
Suppression of inflammatory arthritis by simultaneous inhibition of nitric oxide synthase and NADPH oxidase
Free Radic Biol Med
DiphenylÍeneiodonium inhibits reduction of iron-sulfur clusters in the mitochondrial NADH-ubiquinone oxidoreductase (Complex I)
J Biol Chem
Expression of intercellular adhesion molecule-1 in atherosclerotic plaques
Am J Pathol
An atheroÍgenic diet rapidly induces VCAM-1, a cytokine-regulatable mononuclear leukocyte adhesion molecule, in rabbit aortic endothelium
Arterio Thromb
Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis
Science
Vascular cell adhesion molecule-1 (VCAM-1) gene transcription and expression are regulated through an antioxidant-sensitive mechanism in human vascular endothelial cells
J Clin Invest
Antioxidants inhibit monocyte adhesion by suppressing nuclear factor-kappa B mobilization and induction of vascular cell adhesion molecule-1 in endothelial cells stimulated to generate radicals
Arterio Thromb
Cloning of the human gene for intercellular adhesion molecule 1 and analysis of its 5′-regulatory region. Induction by cytokines and phorbol ester
J Immunol
Reactive oxygen species and vascular signal transduction mechanisms
Microcirculation
Phosphatidic acid as a second messenger in human polymorphonuclear leukocytes. Effects on activation of NADPH oxidase
J Clin Invest
A role for endothelial cell lipoxygenase in the oxidative modification of low density lipoprotein
Proc Natl Acad Sci USA
Hormone- and growth factor-stimulated NADH oxidase
J Bioenerg Biomembr
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ICAM-1 in HIV infection and underlying mechanisms
2020, CytokineSelol (Se IV) modulates adhesive molecules in control and TNF-α-stimulated HMEC-1 cells
2019, Journal of Trace Elements in Medicine and BiologyCitation Excerpt :Surprisingly, we observed decreased VCAM-1 expression in Selol treated cells and opposite effect when Selol and TNF-α were added together. Although ICAM-1 and VCAM-1 play important functions during inflammation and are expressed under the influence of many of the same pro-inflammatory stimuli there is evidence that some factors (cytokines, the cell redox state) can trigger specific mechanisms that allow the expression of one particle independent of the expression of the second [65–68]. The specific regulation of VCAM-1 expression is possible, among others due to the presence in the promoter region of this adhesive particle of motifs allowing the attachment of GATA binding transcription factors (GATA binding proteins) and IRF1 (IF-regulatory factor).
Assessment of Novel Antioxidant Therapy in Atherosclerosis by Contrast Ultrasound Molecular Imaging
2018, Journal of the American Society of EchocardiographyCitation Excerpt :Vascular inflammation occurs through signaling of specific receptors such (lectin-like oxidized low-density lipoprotein receptor, Toll-like receptors, and scavenger receptors)6,9 or inhibition of anti-inflammatory processes.22 As a result, there is upregulation of adhesion molecules including P-selectin, intercellular adhesion molecule–1, and vascular cell adhesion molecule–1 that are involved in leukocyte recruitment and the endothelial production of pro-inflammatory chemokines.4,5 Platelet recruitment is yet another proatherosclerotic consequence of oxidative stress that occurs, in part, from endothelial events.
Redox regulation of cell migration and adhesion
2012, Trends in Cell BiologyCitation Excerpt :Indeed, subsequent experiments demonstrated that TNF-α, as well as two other cytokines, TNF-related activation-induced cytokine (TRANCE) and visfatin, induced a transient increase in ROS levels in endothelial cells. Furthermore, inhibition of NADPH oxidase attenuated this increase in ROS levels, as well as expression of the cell surface adhesion molecules ICAM-1 and vascular cell adhesion molecule 1 (VCAM-1) [13,14,34,72]. In addition to acting through hydrogen peroxide, superoxide itself has been suggested to direct TNF-α-induced surface expression of adhesion molecules because overexpression of SOD1 suppresses this expression [13].
The role of antibody synergy and membrane fluidity in the vascular targeting of immunoliposomes
2010, BiomaterialsCitation Excerpt :Vein ECs and aortic SMCs have been characterized widely and used commonly to study cardiovascular systems. Aortic and vein ECs show qualitatively similar growth, morphology, and response to adhesion molecule modulation [32–36]. We were unable to secure vein smooth muscle cells from Lonza and have continued our study using aortic smooth muscle cells.
An emerging role of deubiquitinating enzyme cylindromatosis (CYLD) in the tubulointerstitial inflammation of IgA nephropathy
2009, Biochemical and Biophysical Research CommunicationsCitation Excerpt :These investigations will create a new avenue to understand the pathogenesis of IgA nephropathy and facilitate development of rational therapeutic strategies for the treatment of this disease. It should be noted that NF-κB as well as mitogen-activated protein kinases (MAPKs) including ERK, p38, and JNK that are critical for TNFα-induced ICAM-1 expression [25,26]; however, engagement of these individual signaling molecules for the ICAM-1 expression is largely dependent the nature of stimulation and/or cell types. In epithelial cells including HK-2 cells, TNFα up-regulates ICAM-1 expression via activation of MAPKs rather than NF-κB [29,30].
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Please address all correspondence to: Xi-Lin Chen MD, PhD, AtheroGenics, Inc8995 Westside Parkway, Alpharetta, GA 30004, USA.