Dexamethasone suppresses iNOS gene expression by inhibiting NF-κB in vascular smooth muscle cells

Matsumura, Mihoko; Kakishita, Hirobumi; Suzuki, Manabu; Banba, Nobuyuki; Hattori, Yoshiyuki

doi:10.1016/s0024-3205(01)01196-1

Cited by 81 publications

(45 citation statements)

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“…Since the promoter region of the iNOS gene contains binding sites for NF-kB and AP-1 (50) , dexamethasone inhibits iNOS expression and NO production by interfering with the NF-kB and/or AP-1 signalling pathways (51,52) . Accordingly, our previous work demonstrated that, in FSDC cells, dexamethasone prevents granulocyte macrophage colony-stimulating factor (GM-CSF)-induced NF-kB activation, iNOS expression, and NO production (53) .…”

Section: Inos Expression By Skin Sensitizers 235mentioning

confidence: 99%

Effect of Skin Sensitizers on Inducible Nitric Oxide Synthase Expression and Nitric Oxide Production in Skin Dendritic Cells: Role of Different Immunosuppressive Drugs

Cruz

Neves

Gonçalo

et al. 2007

Immunopharmacology and Immunotoxicology

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Section: Inos Expression By Skin Sensitizers 235mentioning

confidence: 99%

Effect of Skin Sensitizers on Inducible Nitric Oxide Synthase Expression and Nitric Oxide Production in Skin Dendritic Cells: Role of Different Immunosuppressive Drugs

Cruz

Neves

Gonçalo

et al. 2007

Immunopharmacology and Immunotoxicology

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“…Studies using the candidate gene approach has shown that bacterial lipopolysaccharide induces differential induction of the expression of several VSMC genes that encode cytokines (IL-1 [52] , IL-6 [53] , TNF-alpha [54] , IFN [55] ), chemokines (MCP-1 [56] , IP-10 [57] , IL-8, MIP-2 [58] ), enzymes involved in prostanoid synthesis (PLA2 [59] , COX-2 [60] ), adhesion molecules (VCAM-1 [61] , E-selectin [62] , ICAM-1 [63] ), LPS-binding proteins (LBP [64] , CD14 [65] , TLR4 [17] ), human antigen R 16 (an RNA-binding protein involved in LPS cell activation effects), adrenomedullin [66] , heme oxygenase-1 [67] , low-density lipoprotein receptor-1 (LOX-1) [68] , complement components and regulators (C3, C4, DAF, MCP, CD59 [69] ), iNOS [70] and NO production [71] , endothelin-receptor A and B [72] , antiviral cytomegalovirus inducible gene 5 (viperin) [73] , tissue factor and urokinase-type plasminogen activator (u-PA) [74] . LPS has also been shown to mediate some of its effects by the regulation of cytokines [55] , activation of NADPH oxidase [17] and MAPK [17,75] and NFKB [70] signaling pathways.…”

Section: Structural Proteinsmentioning

confidence: 99%

“…LPS has also been shown to mediate some of its effects by the regulation of cytokines [55] , activation of NADPH oxidase [17] and MAPK [17,75] and NFKB [70] signaling pathways. The data reported in this study is in agreement with most of these findings and also provides a comprehensive list of genes that have thus far not been implicated in LPS biology.…”

Section: Structural Proteinsmentioning

confidence: 99%

Microarray Analysis of Human Vascular Smooth Muscle Cell Responses to Bacterial Lipopolysaccharide

James¹,

Minta²,

Yun³

et al. 2007

American J. of Immunology

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Accumulating evidence suggest a causal role of bacterial and viral infections in atherogenesis. Bacterial lipopolysaccharide (LPS) has been shown to stimulate resting vascular smooth muscle cells (SMC) with the production of inflammatory cytokines and modulation of quiescent cells to the proliferative and synthetic phenotype. To comprehensively identify biologically important genes associated with LPS-induced SMC phenotype modulation, we compared the transcriptomes of quiescent human coronary artery SMC and cells treated with LPS for 4 and 22 h. The SMCs responded robustly to LPS treatment by the differential regulation of several genes involved in chromatin remodeling, transcription regulation, translation, signal transduction, metabolism, host defense, cell proliferation, apoptosis, matrix formation, adhesion and motility and suggest that the induction of clusters of genes involved in cell proliferation, migration and ECM production may be the main force that drives the LPS-induced phenotypic modulation of SMC rather than the differential expression of a single gene or a few genes. An interesting observation was the early and dramatic induction of four tightly clustered interferon-induced genes with tetratricopeptide repeats (IFIT1, 2, 4, 5). siRNA knock-down of IFIT1 in SMC was found to be associated with a remarkable up-regulation of TP53, CDKN1A and FOS, suggesting that IFIT1 may play a role in cell proliferation. Our data provide a comprehensive list of genes involved in LPS biology and underscore the important role of LPS in SMC activation and phenotype modulation which is a pivotal event in the onset of atherogenesis.

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“…Three isoforms of NOS-neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS)-are responsible for NO production. Of these three NOS enzymes, GR represses the expression of iNOS and eNOS [Matsumura et al, 2001;Wallerath et al, 1999]. eNOS constitutively produces NO in the endothelium to serve as a primary control of vascular tone.…”

Section: Vascular Gr Regulation Of Blood Pressurementioning

confidence: 99%

Adrenal corticosteroids, their receptors and hypertension

Hu¹,

Bolten²

2006

Drug Development Research

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Mineralocorticoids and glucocorticoids are primarily synthesized in the adrenal cortex, and play key roles in mediating physiological responses under stressful conditions, such as lack of water or nutrients. Both types of corticosteroid elevate blood pressure and elevated levels of these steroids are found in hypertensive patients. The major mineralocorticoid and glucocorticoid in humans are aldosterone and cortisol, respectively. Aldosterone activates the mineralocorticoid receptor (MR) and cortisol the glucocorticoid receptor (GR). In this overview, the clinical and genetic evidence that both MR and GR are involved in blood pressure regulation is reviewed as are the mechanisms by which MR and GR regulate blood pressure in response to agonists. MR antagonists have been used to treat hypertension. However, GR antagonists have not been fully explored in the clinic. Based on the prevalence of abnormal mineralocorticoid and glucocorticoid signaling in hypertension patients, it is proposed that antagonizing these adrenal corticosteroid receptors will provide benefit in treating hypertension. Drug Dev. Res. 67:871-883, 2006.

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Dexamethasone suppresses iNOS gene expression by inhibiting NF-κB in vascular smooth muscle cells

Cited by 81 publications

References 0 publications

Effect of Skin Sensitizers on Inducible Nitric Oxide Synthase Expression and Nitric Oxide Production in Skin Dendritic Cells: Role of Different Immunosuppressive Drugs

Effect of Skin Sensitizers on Inducible Nitric Oxide Synthase Expression and Nitric Oxide Production in Skin Dendritic Cells: Role of Different Immunosuppressive Drugs

Microarray Analysis of Human Vascular Smooth Muscle Cell Responses to Bacterial Lipopolysaccharide

Adrenal corticosteroids, their receptors and hypertension

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