Vitamin D inhibits the growth of and virulence factor gene expression by Porphyromonas gingivalis and blocks activation of the nuclear factor kappa B transcription factor in monocytes

2015 ◽  
Vol 51 (3) ◽  
pp. 359-365 ◽  
Author(s):  
D. Grenier ◽  
M.-P. Morin ◽  
J. Fournier-Larente ◽  
H. Chen
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Transcription Factor ◽  
Porphyromonas Gingivalis ◽  
Virulence Factor ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Factor Gene ◽  
Nuclear Factor Kappa ◽  
Virulence Factor Gene

scholarly journals Challenges with Methods for Detecting and Studying the Transcription Factor Nuclear Factor Kappa B (NF-κB) in the Central Nervous System

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1335
Author(s):  
Marina Mostafizar ◽  
Claudia Cortes-Pérez ◽  
Wanda Snow ◽  
Jelena Djordjevic ◽  
Aida Adlimoghaddam ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Signaling Pathways ◽  
Quantitative Methods ◽  
Nuclear Factor Kappa B ◽  
Inflammatory Responses ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Regulated Gene Expression ◽  
Transcription Factor Nuclear Factor

The transcription factor nuclear factor kappa B (NF-κB) is highly expressed in almost all types of cells. NF-κB is involved in many complex biological processes, in particular in immunity. The activation of the NF-κB signaling pathways is also associated with cancer, diabetes, neurological disorders and even memory. Hence, NF-κB is a central factor for understanding not only fundamental biological presence but also pathogenesis, and has been the subject of intense study in these contexts. Under healthy physiological conditions, the NF-κB pathway promotes synapse growth and synaptic plasticity in neurons, while in glia, NF-κB signaling can promote pro-inflammatory responses to injury. In addition, NF-κB promotes the maintenance and maturation of B cells regulating gene expression in a majority of diverse signaling pathways. Given this, the protein plays a predominant role in activating the mammalian immune system, where NF-κB-regulated gene expression targets processes of inflammation and host defense. Thus, an understanding of the methodological issues around its detection for localization, quantification, and mechanistic insights should have a broad interest across the molecular neuroscience community. In this review, we summarize the available methods for the proper detection and analysis of NF-κB among various brain tissues, cell types, and subcellular compartments, using both qualitative and quantitative methods. We also summarize the flexibility and performance of these experimental methods for the detection of the protein, accurate quantification in different samples, and the experimental challenges in this regard, as well as suggestions to overcome common challenges.

Effect of curcumin on growth, biofilm formation and virulence factor gene expression of Porphyromonas gingivalis

Odontology ◽  
2020 ◽  
Vol 109 (1) ◽  
pp. 18-28
Author(s):  
Vijay M. Kumbar ◽  
Malleswara Rao Peram ◽  
Manohar S. Kugaji ◽  
Tejas Shah ◽  
Sanjivani P. Patil ◽  
...  
Keyword(s):  
Gene Expression ◽  
Porphyromonas Gingivalis ◽  
Virulence Factor ◽  
Biofilm Formation ◽  
Factor Gene ◽  
Virulence Factor Gene

Regulation of endothelial thrombomodulin expression by inflammatory cytokines is mediated by activation of nuclear factor-kappa B

Blood ◽  
2005 ◽  
Vol 105 (10) ◽  
pp. 3910-3917 ◽  
Author(s):  
Richard H. Sohn ◽  
Clayton B. Deming ◽  
David C. Johns ◽  
Hunter C. Champion ◽  
Ce Bian ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Inflammatory Cytokines ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Mobility Shift ◽  
Factor Binding ◽  
Nuclear Factor Kappa ◽  
Tnf Α

AbstractInflammation and thrombosis are increasingly recognized as interrelated biologic processes. Endothelial cell expression of thrombomodulin (TM), a key component of the anticoagulant protein C pathway, is potently inhibited by inflammatory cytokines. Because the mechanism underlying this effect is largely unknown, we investigated a potential role for the inflammatory transcription factor nuclear factor-kappa B (NF-κB). Blocking NF-κB activation effectively prevented cytokine-induced down-regulation of TM, both in vitro and in a mouse model of tumor necrosis factor-α (TNF-α)–mediated lung injury. Although the TM promoter lacks a classic NF-κB consensus site, it does contain tandem Ets transcription factor binding sites previously shown to be important for both constitutive TM gene expression and cytokine-induced repression. Using electrophoretic mobility shift assay and chromatin immunoprecipitation, we found that multiple Ets species bind to the TNF-α response element within the TM promoter. Although cytokine exposure did not alter Ets factor binding, it did reduce binding of p300, a coactivator required by Ets for full transcriptional activity. Overexpression of p300 also prevented TM repression by cytokines. We conclude that NF-κB is a critical mediator of TM repression by cytokines. Further evidence suggests a mechanism involving competition by NF-κB for limited pools of the transcriptional coactivator p300 necessary for TM gene expression.

scholarly journals Vitamin C Activates Osteoblastogenesis and Inhibits Osteoclastogenesis via Wnt/β-Catenin/ATF4 Signaling Pathways

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 506 ◽  
Author(s):  
Hyeon Choi ◽  
Gyeong-Ji Kim ◽  
Han-Seok Yoo ◽  
Da Song ◽  
Kang-Hyun Chung ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Vitamin C ◽  
Signaling Pathways ◽  
Nuclear Factor Kappa B ◽  
Type I ◽  
Nuclear Factor ◽  
Mineral Density ◽  
Nuclear Factor Kappa ◽  
Ovx Rats ◽  
Receptor Activator

This study evaluated the effects of vitamin C on osteogenic differentiation and osteoclast formation, and the effects of vitamin C concentration on bone microstructure in ovariectomized (OVX) Wistar rats. Micro-computed tomography analysis revealed the recovery of bone mineral density and bone separation in OVX rats treated with vitamin C. Histomorphometrical analysis revealed improvements in the number of osteoblasts, osteoclasts, and osteocytes; the osteoblast and osteoclast surface per bone surface; and bone volume in vitamin C-treated OVX rats. The vitamin C-treated group additionally displayed an increase in the expression of osteoblast differentiation genes, including bone morphogenetic protein-2, small mothers against decapentaplegic 1/5/8, runt-related transcription factor 2, osteocalcin, and type I collagen. Vitamin C reduced the expression of osteoclast differentiation genes, such as receptor activator of nuclear factor kappa-B, receptor activator of nuclear factor kappa-B ligand, tartrate-resistant acid phosphatase, and cathepsin K. This study is the first to show that vitamin C can inhibit osteoporosis by promoting osteoblast formation and blocking osteoclastogenesis through the activation of wingless-type MMTV integration site family/β-catenin/activating transcription factor 4 signaling, which is achieved through the serine/threonine kinase and mitogen-activated protein kinase signaling pathways. Therefore, our results suggest that vitamin C improves bone regeneration.

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