Regulation of NF-κB-dependent Gene Expression by the POU Domain Transcription Factor Oct-1

Paz, Nathaniel G. dela; Simeonidis, Simos; Leo, Christopher; Rose, David W.; Collins, Tucker

doi:10.1074/jbc.m606923200

Cited by 51 publications

(16 citation statements)

References 63 publications

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“…Oct-1 is known to have both activating (Duncliffe et al, 1997; Fletcher et al, 1987; Zhou et al, 2007) and silencing activity (dela Paz et al, 2007; Kakizawa et al, 2001; Schwachtgen et al, 1998). Moreover, Oct-1 has been suggested to be a regulatable stabilizer of repressed and inducible transcriptional states (Shakya et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Oct-1 Regulates IL-17 Expression by Directing Interchromosomal Associations in Conjunction with CTCF in T Cells

et al. 2014

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Summary Interchromosomal associations can regulate gene expression but little is known about the molecular basis of such associations. In response to antigen stimulation, naïve T cells can differentiate into Th1, Th2 and Th17 cells expressing IFN-γ, IL-4 and IL-17, respectively. We previously reported that in naïve T cells, the IFN-γ locus is associated with the Th2 cytokine locus. Here we show that the Th2 locus additionally associates with the IL-17 locus. This association requires a DNase I hypersensitive region (RHS6) at the Th2 locus. RHS6 and the IL-17 promoter both bear Oct-1 binding sites. Deletion of either of these sites or Oct-1 gene impairs the association. Oct-1 and CTCF bind their cognate sites cooperatively and CTCF-deficiency similarly impairs the association. Finally, defects in the association lead to enhanced IL-17 induction. Collectively, our data indicate Th17 lineage differentiation is restrained by the Th2 locus via interchromosomal associations organized by Oct-1 and CTCF.

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Section: Discussionmentioning

confidence: 99%

Oct-1 Regulates IL-17 Expression by Directing Interchromosomal Associations in Conjunction with CTCF in T Cells

et al. 2014

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“…Furthermore, TNF-α stimulates endothelial generation of reactive oxygen species by activating the NADPH oxidase subunits gp91 phox, NOX-1, p47phox, and p22phox. TNF-α also activates the transcription of NF-κB, which regulates the expression of genes involved in inflammation, oxidative stress and endothelial dysfunction 11,38…”

Section: Discussionmentioning

confidence: 99%

Rosuvastatin prevents proteinuria and renal inflammation in nitric oxide–deficient rats

Girardi

Farias

Ferreira

et al. 2011

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OBJECTIVE:The aim of the present study was to assess the effects of rosuvastatin on renal injury and inflammation in a model of nitric oxide deficiency.METHODS:Male Wistar rats were randomly divided into four groups (n = 10/group) and treated for 28 days with saline (CTRL); 30 mg/kg/day L-NAME (L-name); L-NAME and 20 mg/kg/day rosuvastatin (L-name+ROS-20); or L-NAME and 2 mg/kg/day rosuvastatin (L-name+ROS-2). Systolic blood pressure was measured by plethysmography in the central artery of the tail. The serum total cholesterol, triglycerides, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, creatinine, nitric oxide, interleukin-6, and tumor necrosis factor alpha levels were analyzed. Urine samples were taken to measure the albumin∶urinary creatinine ratio. Kidneys were sectioned and stained with hematoxylin/eosin and Masson's trichrome. Immunohistochemical analysis of the renal tissue was performed to detect macrophage infiltration of the glomeruli.RESULTS:The systolic blood pressure was elevated in the L-name but not the L-name+rosuvastatin-20 and L-name+rosuvastatin-2 groups. The L-name group had a significantly reduced nitric oxide level and an increased interleukin-6 and tumor necrosis factor alpha level, albumin∶urinary creatinine ratio and number of macrophages in the renal glomeruli. Rosuvastatin increased the nitric oxide level in the L-name+rosuvastatin-2 group and reduced the interleukin-6 and tumor necrosis factor alpha levels, glomerular macrophage number and albumin∶urinary creatinine ratio in the L-name+rosuvastatin-20 and L-name+rosuvastatin-2 groups.CONCLUSION:Rosuvastatin treatment reduced glomerular damage due to improvement in the inflammatory pattern independent of the systolic blood pressure and serum lipid level. These effects may lead to improvements in the treatment of kidney disease.

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“…TNF-α activates the transcription of NF-κB, which regulates the expression of genes involved in inflammation, oxidative stress and endothelial dysfunction [51–53]. TNF-α initiates the signalling cascades via the IKK [IκB (inhibitor of NF-κB) kinase] complex, which contains IKKα and IKKβ.…”

Section: Effect Of Tnf-α On Ros Productionmentioning

confidence: 99%

Role of TNF-α in vascular dysfunction

et al. 2009

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Healthy vascular function is primarily regulated by several factors including EDRF (endothelium-dependent relaxing factor), EDCF (endothelium-dependent contracting factor) and EDHF (endothelium-dependent hyperpolarizing factor). Vascular dysfunction or injury induced by aging, smoking, inflammation, trauma, hyperlipidaemia and hyperglycaemia are among a myriad of risk factors that may contribute to the pathogenesis of many cardiovascular diseases, such as hypertension, diabetes and atherosclerosis. However, the exact mechanisms underlying the impaired vascular activity remain unresolved and there is no current scientific consensus. Accumulating evidence suggests that the inflammatory cytokine TNF (tumour necrosis factor)-α plays a pivotal role in the disruption of macrovascular and microvascular circulation both in vivo and in vitro. AGEs (advanced glycation end-products)/RAGE (receptor for AGEs), LOX-1 [lectin-like oxidized low-density lipoprotein receptor-1) and NF-κB (nuclear factor κB) signalling play key roles in TNF-α expression through an increase in circulating and/or local vascular TNF-α production. The increase in TNF-α expression induces the production of ROS (reactive oxygen species), resulting in endothelial dysfunction in many pathophysiological conditions. Lipid metabolism, dietary supplements and physical activity affect TNF-α expression. The interaction between TNF-α and stem cells is also important in terms of vascular repair or regeneration. Careful scrutiny of these factors may help elucidate the mechanisms that induce vascular dysfunction. The focus of the present review is to summarize recent evidence showing the role of TNF-α in vascular dysfunction in cardiovascular disease. We believe these findings may prompt new directions for targeting inflammation in future therapies.

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Regulation of NF-κB-dependent Gene Expression by the POU Domain Transcription Factor Oct-1

Abstract: Maintenance of the cells of the vessel wall in a quiescent

Cited by 51 publications

References 63 publications

Oct-1 Regulates IL-17 Expression by Directing Interchromosomal Associations in Conjunction with CTCF in T Cells

Oct-1 Regulates IL-17 Expression by Directing Interchromosomal Associations in Conjunction with CTCF in T Cells

Rosuvastatin prevents proteinuria and renal inflammation in nitric oxide–deficient rats

Role of TNF-α in vascular dysfunction

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