Penta-O-galloyl-β-d-glucose inhibits phorbol myristate acetate-induced intereukin-8 gene expression in human monocytic U937 cells through its inactivation of nuclear factor-κB

AbstractThis work investigated the functional role of nuclear factor–κB (NF-κB) in respiratory burst activity and in expression of the human phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase genes CYBB, CYBA, NCF1, and NCF2. U937 cells with a stably transfected repressor of NF-κB (IκBα-S32A/S36A) demonstrated significantly lower superoxide release and lower CYBB and NCF1 gene expression compared with control U937 cells. We further tested Epstein-Barr virus (EBV)-transformed B cells from patients with anhidrotic ectodermal dysplasia with immunodeficiency (EDA-ID), an inherited disorder of NF-κB function. Superoxide release and CYBB gene expression by EDA-ID cells were significantly decreased compared with healthy cells and similar to cells from patients with X-linked chronic granulomatous disease (X910 CGD). NCF1 gene expression in EDA-ID S32I cells was decreased compared with healthy control cells and similar to that in autosomal recessive (A470) CGD cells. Gel shift assays demonstrated loss of recombinant human p50 binding to a NF-κB site 5′ to the CYBB gene in U937 cells treated with NF-κB inhibitors, repressor-transfected U937 cells, and EDA-ID patients' cells. Zymosan phagocytosis was not affected by transfection of U937 cells with the NF-κB repressor. These studies show that NF-κB is necessary for CYBB and NCF1 gene expression and activation of the phagocyte NADPH oxidase in this model system.

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Osteopontin is associated with nuclear factor κB gene expression during tail-suspension-induced bone loss

Experimental Cell Research ◽

10.1016/j.yexcr.2006.06.003 ◽

2006 ◽

Vol 312 (16) ◽

pp. 3075-3083 ◽

Cited By ~ 32

Author(s):

Muneaki Ishijima ◽

Yoichi Ezura ◽

Kunikazu Tsuji ◽

Susan R. Rittling ◽

Hisashi Kurosawa ◽

...

Keyword(s):

Gene Expression ◽

Bone Loss ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

Tail Suspension

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Activation of Nuclear Factor κb and bcl-x Survival Gene Expression by Nerve Growth Factor Requires Tyrosine Phosphorylation of IκBα

The Journal of Cell Biology ◽

10.1083/jcb.152.4.753 ◽

2001 ◽

Vol 152 (4) ◽

pp. 753-764 ◽

Cited By ~ 100

Author(s):

Nguyen Truc Bui ◽

Antonia Livolsi ◽

Jean-Francois Peyron ◽

Jochen H.M. Prehn

Keyword(s):

Gene Expression ◽

Tyrosine Phosphorylation ◽

Fluorescent Protein ◽

Nuclear Translocation ◽

Nuclear Factor Κb ◽

Dominant Negative ◽

Dominant Negative Mutant ◽

Nuclear Factor ◽

Human Neuroblastoma ◽

Tnf Α

NGF has been shown to support neuron survival by activating the transcription factor nuclear factor-κB (NFκB). We investigated the effect of NGF on the expression of Bcl-xL, an anti–apoptotic Bcl-2 family protein. Treatment of rat pheochromocytoma PC12 cells, human neuroblastoma SH-SY5Y cells, or primary rat hippocampal neurons with NGF (0.1–10 ng/ml) increased the expression of bcl-xL mRNA and protein. Reporter gene analysis revealed a significant increase in NFκB activity after treatment with NGF that was associated with increased nuclear translocation of the active NFκB p65 subunit. NGF-induced NFκB activity and Bcl-xL expression were inhibited in cells overexpressing the NFκB inhibitor, IκBα. Unlike tumor necrosis factor-α (TNF-α), however, NGF-induced NFκB activation occurred without significant degradation of IκBs determined by Western blot analysis and time-lapse imaging of neurons expressing green fluorescent protein–tagged IκBα. Moreover, in contrast to TNF-α, NGF failed to phosphorylate IκBα at serine residue 32, but instead caused significant tyrosine phosphorylation. Overexpression of a Y42F mutant of IκBα potently suppressed NFG-, but not TNF-α–induced NFκB activation. Conversely, overexpression of a dominant negative mutant of TNF receptor-associated factor-6 blocked TNF-α–, but not NGF-induced NFκB activation. We conclude that NGF and TNF-α induce different signaling pathways in neurons to activate NFκB and bcl-x gene expression.

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Oxidative Stress-Dependent Impairment of Cardiac-Specific Transcription Factors in Experimental Diabetes

Endocrinology ◽

10.1210/en.2006-0728 ◽

2006 ◽

Vol 147 (12) ◽

pp. 5967-5974 ◽

Cited By ~ 73

Author(s):

Manuela Aragno ◽

Raffaella Mastrocola ◽

Claudio Medana ◽

Maria Graziella Catalano ◽

Ilenia Vercellinatto ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Left Ventricle ◽

Nuclear Factor Κb ◽

Diabetic Rats ◽

Nuclear Factor ◽

Downstream Signaling ◽

Zdf Rats ◽

Myogenic Factors ◽

Age Receptors

Oxidative stress plays a key role in the pathogenesis of diabetic cardiomyopathy, which is characterized by myocyte loss and fibrosis, finally resulting in heart failure. The study looked at the downstream signaling whereby oxidative stress leads to reduced myocardial contractility in the left ventricle of diabetic rats and the effects of dehydroepiandrosterone (DHEA), which production is suppressed in the failing heart and prevents the oxidative damage induced by hyperglycemia in several experimental models. DHEA was given orally at a dose of 4 mg/rat per day for 21 d to rats with streptozotocin (STZ)-induced diabetes and genetic diabetic-fatty (ZDF) rats. Oxidative balance, advanced glycated end products (AGEs) and AGE receptors, cardiac myogenic factors, and myosin heavy-chain gene expression were determined in the left ventricle of treated and untreated STZ-diabetic rats and ZDF rats. Oxidative stress induced by chronic hyperglycemia increased AGE and AGE receptors and led to activation of the pleoitropic transcription factor nuclear factor-κB. Nuclear factor-κB activation triggered a cascade of signaling, which finally led to the switch in the cardiac myosin heavy-chain (MHC) gene expression from the α-MHC isoform to the β-MHC isoform. DHEA treatment, by preventing the activation of the oxidative pathways induced by hyperglycemia, counteracted the enhanced AGE receptor activation in the heart of STZ-diabetic rats and ZDF rats and normalized downstream signaling, thus avoiding impairment of the cardiac myogenic factors, heart autonomic nervous system and neural crest derivatives (HAND) and myogenic enhancer factor-2, and the switch in MHC gene expression, which are the early events in diabetic cardiomyopathy.

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Plant extracts of spices and coffee synergistically dampen nuclear factor–κB in U937 cells

Nutrition Research ◽

10.1016/j.nutres.2013.07.008 ◽

2013 ◽

Vol 33 (10) ◽

pp. 817-830 ◽

Cited By ~ 5

Author(s):

Marit Kolberg ◽

Ingvild Paur ◽

Trude R. Balstad ◽

Sigrid Pedersen ◽

David R. Jacobs ◽

...

Keyword(s):

Plant Extracts ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

U937 Cells

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Effects of Acute γ-Hexachlorocyclohexane Intoxication in Relation to the Redox Regulation of Nuclear Factor-κB, Cytokine Gene Expression, and Liver Injury in the Rat

Antioxidants and Redox Signaling ◽

10.1089/152308604322899530 ◽

2004 ◽

Vol 6 (2) ◽

pp. 471-480 ◽

Cited By ~ 12

Author(s):

Luis A. Videla ◽

Gladys Tapia ◽

Patricia Varela ◽

Pamela Cornejo ◽

Julia Guerrero ◽

...

Keyword(s):

Gene Expression ◽

Liver Injury ◽

Redox Regulation ◽

Nuclear Factor Κb ◽

Cytokine Gene Expression ◽

Nuclear Factor ◽

Cytokine Gene

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Regulation of intercellular adhesion molecule-1 gene expression involves multiple mRNA stabilization mechanisms: effects of interferon- gamma and phorbol myristate acetate

Blood ◽

10.1182/blood.v84.8.2632.2632 ◽

1994 ◽

Vol 84 (8) ◽

pp. 2632-2639 ◽

Cited By ~ 24

Author(s):

M Ohh ◽

CA Smith ◽

C Carpenito ◽

F Takei

Keyword(s):

Gene Expression ◽

Interferon Gamma ◽

Adhesion Molecule ◽

Phorbol Myristate Acetate ◽

Full Length ◽

Intercellular Adhesion Molecule ◽

Myristate Acetate ◽

Intercellular Adhesion Molecule 1 ◽

Ifn Gamma ◽

Mrna Stabilization

Abstract Although the intercellular adhesion molecule-1 (ICAM-1) is constitutively expressed at a low level on a subpopulation of hematopoietic cells, on vascular endothelium, on fibroblasts, and on certain epithelial cells, it is dramatically increased at sites of inflammation. Interferon-gamma (IFN-gamma) and phorbol myristate acetate (PMA) are known to increase the expression of ICAM-1 on many cell types. Because both human and murine ICAM-1 mRNAs contain putative destabilizing AUUUA sequences in their 3′ untranslated regions (UTRs), we examined the role of mRNA stability in the regulation of ICAM-1 gene expression. The treatment of the murine monocytic cell line P388D1, which constitutively expresses ICAM-1 mRNA at a low level, with IFN- gamma or PMA rapidly enhanced the level of ICAM-1 mRNA and dramatically prolonged its half-life. To determine whether the putative destabilizing sequences are responsible for this effect of IFN-gamma and PMA, fibroblast L cells were transfected with either the full- length ICAM-1 cDNA or a truncated form (ICAM-1 delta 3) lacking the putative destabilizing AUUUA sequences. Although ICAM-1 delta 3 mRNA was more stable than the full-length ICAM-1 mRNA, IFN-gamma treatment induced the accumulation of both mRNA species and prolongation of their half-lives. The transplantation of the ICAM-1 delta 3′ UTR into a stable ICAM-2 mRNA rendered it unstable, and it was unresponsive to IFN- gamma. Therefore, the treatment with IFN-gamma stabilizes the otherwise labile ICAM-1 mRNA, but the IFN-gamma-responsive sequence may at least in part reside within the protein coding region. PMA also upregulated ICAM-1 gene expression by mRNA stabilization. However, unlike IFN- gamma, PMA treatment only increased the level of the full-length, but not of the truncated, ICAM-1 mRNA. This shows that the PMA-responsive element is located within the 3′UTR. Furthermore, the effect of PMA on ICAM-1 delta 3 mRNA was recovered by ligating multiple AUUUA sequences derived from a heterologous gene fragment. The stability of this chimeric mRNA and the full-length ICAM-1 mRNA was markedly increased by PMA treatment, indicating that the AUUUA multimers in the 3′UTR are important in the PMA-induced upregulation of ICAM-1 mRNA.

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