Intercellular Adhesion Molecule 1 (ICAM-1) is Synergistically Activated by TNF-α and IFN-γ Responsive Sites

Jahnke, Andreas; Johnson, Judith P.

doi:10.1016/s0171-2985(11)80559-0

Cited by 31 publications

(19 citation statements)

References 31 publications

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“…The majority of promoters induced synergistically by IFN-␥ and TNF-␣ contain binding sites for STAT1 or IRF-1 and NF-B (Paludan, 2000). A number of studies have demonstrated synergy between STAT1 and NF-B (Jahnke and Johnson, 1995;Krzesz et al, 1999). Indeed, a recent study demonstrated that in rat aortic smooth muscle cells TNF-␣, via activation of NF-B, and IFN-␥, via activation of STAT, up-regulate CD40 gene expression (Krzesz et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Role for Nuclear Factor-κB and Signal Transducer and Activator of Transcription 1/Interferon Regulatory Factor-1 in Cytokine-Induced Endothelin-1 Release in Human Vascular Smooth Muscle Cells

Woods¹,

Wood²,

Bardswell³

et al. 2003

Mol Pharmacol

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Endothelin-1 (ET-1) is a potent vasoconstrictor and growthpromoting mediator that is involved in the maintenance of vascular tone within the healthy circulation. However, a pathogenic role has been implicated by its overproduction in a number of cardiovascular diseases, which include pulmonary hypertension, congestive heart failure, atherosclerosis, and coronary vasospasm. ET-1 mRNA expression and peptide production in human vascular smooth muscle cells (HVSMCs) are markedly increased by exposure to tumor necrosis factor-␣ and interferon-␥. The intracellular signaling mechanism involved in this pathway is not known.

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Section: Discussionmentioning

confidence: 99%

Role for Nuclear Factor-κB and Signal Transducer and Activator of Transcription 1/Interferon Regulatory Factor-1 in Cytokine-Induced Endothelin-1 Release in Human Vascular Smooth Muscle Cells

Woods¹,

Wood²,

Bardswell³

et al. 2003

Mol Pharmacol

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“…Furthermore, both cytokines collaborate at the gene level by increasing promoter activation through a synergistic interaction between transcription factors activated by IFN-g (STATs) and TNF-a (NF-kB). Thus, a functional cooperation has been demonstrated between NF-kB and STAT1 in the regulation of genes activated by IFN-g and TNF-a, including ICAM-1 (25), RANTES (regulated on activation, normal T cells expressed and secreted) (26), and Caspase 11 (27). Recent evidence also showed that STATs cooperatively interact with IRF-1 to regulate gene transcription by involving multiple mechanisms.…”

Section: Signaling Cross Talk Between Ifn-g and Other Pro-asthmatic Cmentioning

confidence: 99%

Airway Smooth Muscle Cell as an Inflammatory Cell: Lessons Learned from Interferon Signaling Pathways

Tliba¹,

Amrani²

2008

Proceedings of the American Thoracic Society

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The present article will describe the potential role of airway smooth muscle (ASM) in mediating both deleterious/beneficial effects of interferons (IFNs) in asthma. First described as beneficial in treating the main features of asthma, the interplay between IFNs and ASM could explain their deleterious actions recently described in a number of different studies. Through multiple mechanisms, including the suppression of steroid action, the synergistic pro-inflammatory actions when combined with other cytokines, and the modulation of calcium metabolism, IFNs are now seen as critical mediators in the pathogenesis of asthma.

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“…Recent evidence indicates that the ICAM-1 promotor is dependent on p65 homodimers that bind to a variant kappa B site in cytokine-activated endothelial cells [16,18]. The dependence of cytokine-induced ICAM-1 expression on NF-kappa activation is supported by data showing that antioxidant inhibitors of NF-kB, such as pyrrolidine dithiocarbamate, dramatically attenuate ICAM-1 gene expression [19].…”

Section: Introductionmentioning

confidence: 99%

Colonic epithelial cells induce endothelial cell expression of ICAM-1 and VCAM-1 by a NF-κB-dependent mechanism

Maaser¹,

Schoeppner²,

Kucharzik³

et al. 2001

Clinical and Experimental Immunology

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SUMMARYEpithelial cells are positioned in close proximity to endothelial cells. A non-contact coculture system was used to investigate whether colonic epithelial cells activated with various cytokines are able to provide signals that can modulate ICAM-1 and VCAM-1 expression on endothelial cells. Coculture of human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC-1) with TNF-a /IFN-g-stimulated human colon epithelial cell lines led to a significant up-regulation of endothelial ICAM-1 and VCAM-1 expression. Increased ICAM-1 and VCAM-1 expression by endothelial cells was accompanied by an increase in endothelial cell NF-kB p65 and NF-kB-DNAbinding activity. Inhibition of endothelial NF-kB activation using the proteosome inhibitors MG-132 and BAY 11±7082 resulted in a significant decrease of ICAM-1 expression, indicating an important role for NF-kB in this response. This cross-talk may represent a biological mechanism for the gut epithelium to control the colonic inflammatory response and the subsequent immune cell recruitment during inflammation.

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Intercellular Adhesion Molecule 1 (ICAM-1) is Synergistically Activated by TNF-α and IFN-γ Responsive Sites

Cited by 31 publications

References 31 publications

Role for Nuclear Factor-κB and Signal Transducer and Activator of Transcription 1/Interferon Regulatory Factor-1 in Cytokine-Induced Endothelin-1 Release in Human Vascular Smooth Muscle Cells

Role for Nuclear Factor-κB and Signal Transducer and Activator of Transcription 1/Interferon Regulatory Factor-1 in Cytokine-Induced Endothelin-1 Release in Human Vascular Smooth Muscle Cells

Airway Smooth Muscle Cell as an Inflammatory Cell: Lessons Learned from Interferon Signaling Pathways

Colonic epithelial cells induce endothelial cell expression of ICAM-1 and VCAM-1 by a NF-κB-dependent mechanism

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