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Start Over Author "Liu, Jiqin" Topic nf-kappa b
3 results on '"Liu, Jiqin"'

1. Thymocytes are activated by toluene inhalation through the transcription factors NF-κB, STAT5 and NF-AT.

Author

Liu J, Yoshida Y, Kunugita N, Noguchi J, Sugiura T, Ding N, Arashidani K, Fujimaki H, and Yamashita U

Subjects
Administration, Inhalation, Animals, Cells, Cultured, Dose-Response Relationship, Drug, Interleukin-2 biosynthesis, Interleukin-2 immunology, Male, Mice, Mice, Inbred C3H, Time Factors, Toluene administration & dosage, Lymphocyte Activation immunology, NF-kappa B physiology, NFATC Transcription Factors physiology, STAT5 Transcription Factor physiology, T-Lymphocytes drug effects, T-Lymphocytes immunology, Thymus Gland cytology, Toluene pharmacology
Abstract

Toluene has been extensively examined for effects on the central nervous system. To investigate the influence of low-level inhalation of toluene on the naive immune cells, male C3H/HeN mice were exposed to filtered air (control) and 50 ppm of toluene for 3 weeks. Low-level exposure resulted in (1) increased proliferation of thymocytes, (2) IL-2 production induced in thymocytes and (3) activation of the transcription factors NF-κB, STAT5 and NF-AT in thymocytes. These results suggest that thymocytes are sensitive cells and T cell activators are candidates for biomarkers for low-level exposure to toluene on naive immune cells., (Copyright © 2010 John Wiley & Sons, Ltd.)

Published
2010
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2. DNA-binding activity of NF-kappaB and phosphorylation of p65 are induced by N-acetylcysteine through phosphatidylinositol (PI) 3-kinase.

Author

Liu J, Yoshida Y, and Yamashita U

Subjects
Active Transport, Cell Nucleus, Agammaglobulinaemia Tyrosine Kinase, Ascorbic Acid metabolism, Ascorbic Acid pharmacology, Cell Line, Cell Nucleus metabolism, Humans, NF-kappa B antagonists & inhibitors, Phosphorylation, Protein Binding, Protein-Tyrosine Kinases antagonists & inhibitors, Reactive Oxygen Species metabolism, Signal Transduction, Thiourea analogs & derivatives, Thiourea pharmacology, Transcription Factor RelA antagonists & inhibitors, Transcription Factor RelA metabolism, Acetylcysteine pharmacology, Antioxidants pharmacology, DNA metabolism, NF-kappa B metabolism, Phosphatidylinositol 3-Kinases physiology
Abstract

N-Acetylcysteine (NAC) has been widely used as an antioxidant in research, however, it has also been found to reduce the binding of TNF to its receptor independent of its antioxidative role. In this study, we investigated the effect of NAC on NF-kappaB activation. In HeLa cells, Hep3B cells, and A549 cells, DNA-binding activity of NF-kappaB was induced by NAC without any other stimulation but not by tetramethylthiourea (TMTU) or vitamin C, suggesting that ROS is not involved in the effect of NAC. The degradation of IkappaBalpha and nuclear translocation of NF-kappaB were not induced by NAC. The phosphorylation of p65 at serine 536 was induced by NAC, which is known to contribute to the enhancement of DNA-binding activity of NF-kappaB, however, NAC did not directly phosphorylate p65. The NAC-induced DNA-binding activity of NF-kappaB and phosphorylation of p65 were sensitive to a phosphatidylinositol (PI) 3-kinase inhibitor, partially sensitive to an IkappaB kinase (IKK) inhibitor, but not sensitive to a Bruton's tyrosine kinase (Btk) inhibitor. Moreover, both the DNA-binding activity and phosphorylation induced by NAC were reduced by the overexpression of a dominant negative Akt in HeLa cells. These results suggest that NAC activates mainly PI3K to phosphorylate p65 and subsequently induces DNA-binding activity of NF-kappaB, independent of its antioxidative function.

Published
2008
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3. ROS-induced ZNF580 expression: a key role for H2O2/NF-κB signaling pathway in vascular endothelial inflammation

Author

Wang HeKong, Ren Dang-li, Zhang MingHua, Zhang Wen-cheng, and Liu JiQin

Subjects
Endothelium, medicine.medical_treatment, Clinical Biochemistry, Biology, chemistry.chemical_compound, Pyrrolidine dithiocarbamate, Cell Line, Tumor, medicine, Humans, Molecular Biology, Transcription factor, chemistry.chemical_classification, Inflammation, Reactive oxygen species, Interleukin-8, NF-kappa B, NF-κB, Cell Biology, General Medicine, Hydrogen Peroxide, Molecular biology, Cell biology, Up-Regulation, Endothelial stem cell, medicine.anatomical_structure, Cytokine, chemistry, Endothelium, Vascular, Signal transduction, Reactive Oxygen Species, Signal Transduction, Transcription Factors
Abstract

ZNF580, a newly found C2H2 zinc finger transcription factor, was first described by Zhang (GenBank ID: AF184939). Emerging evidence has suggested that reactive oxygen species (ROS) play an important role in redox-sensitive signal transduction, and the vascular endothelium plays a critical role in the vascular inflammatory response. In this communication, we present evidence for the potential role of ZNF580 in hydrogen peroxide (H2O2)-regulated inflammation-related signaling pathways. In a human endothelial cell hybridoma line (EA.hy926), ZNF580 levels were markedly upregulated with H2O2 stimulation in different concentrations (0–400 μM) and at different time-points (0–6 h). H2O2 promoted the rapid translocation of p65 from the cytoplasm into the nucleus according to immunocytochemistry staining. In subsequent research, inhibition of NF-κB by pyrrolidine dithiocarbamate (PDTC, a selective chemical inhibitor of NF-κB) was shown to block the upregulated expression of ZNF580 that was induced by H2O2. Furthermore, transient transfection of ZNF580 resulted in an increase of the pro-inflammatory cytokine interleukin-8 (IL-8) 3.01 ± 0.05 folds according to real-time RT-PCR and ELISA assays, which also showed significantly enhanced motility of human acute monocytic leukemia cells (THP-1). These results suggest that H2O2 upregulates the expression of ZNF580 via the NF-κB signaling pathway, and overexpression of ZNF580 plays a critical role in augmenting the release of pro-inflammatory cytokine IL-8.

Published
2011

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