Constitutive Activation and Environmental Chemical Induction of the Aryl Hydrocarbon Receptor/Transcription Factor in Activated Human B Lymphocytes

2005 ◽  
Vol 67 (5) ◽  
pp. 1740-1750 ◽  
Author(s):  
Lenka L. Allan ◽  
David H. Sherr
Keyword(s):  
Transcription Factor ◽  
Aryl Hydrocarbon Receptor ◽  
B Lymphocytes ◽  
Chemical Induction ◽  
Environmental Chemical ◽  
Constitutive Activation ◽  
Aryl Hydrocarbon

scholarly journals Aryl Hydrocarbon Receptor Connects Inflammation to Breast Cancer

2020 ◽  
Vol 21 (15) ◽  
pp. 5264 ◽  
Author(s):  
Tiziana Guarnieri
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Immune System ◽  
Aryl Hydrocarbon Receptor ◽  
Inflammatory Marker ◽  
Eukaryotic Cells ◽  
Breast Carcinogenesis ◽  
Constitutive Activation ◽  
Aryl Hydrocarbon ◽  
Over Time

Aryl hydrocarbon receptor (AhR), an evolutionary conserved transcription factor, is a pleiotropic signal transductor. Thanks to its promiscuous ligand binding domain, during the evolution of eukaryotic cells its developmental functions were integrated with biosensor functions. Its activation by a multitude of endogenous and exogenous molecules stimulates its participation in several pathways, some of which are linked to inflammation and breast cancer (BC). Over time, the study of this malignancy has led to the identification of several therapeutic targets in cancer cells. An intense area of study is dedicated to BC phenotypes lacking adequate targets. In this context, due to its high constitutive activation in BC, AhR is currently gaining more and more attention. In this review, I have considered its interactions with: 1. the immune system, whose dysregulation is a renowned cancer hallmark; 2. interleukin 6 (IL6) which is a pivotal inflammatory marker and is closely correlated to breast cancer risk; 3. NF-kB, another evolutionary conserved transcription factor, which plays a key role in immunoregulatory functions, inflammatory response and breast carcinogenesis; 4. kynurenine, a tryptophan-derived ligand that activates and bridges AhR to chronic inflammation and breast carcinogenesis. Overall, the data here presented form an interesting framework where AhR is an interesting connector between inflammation and BC.

Polycyclic Aromatic Hydrocarbons Can Trigger Hepatocyte Release of Extracellular Vesicles by Various Mechanisms of Action Depending on Their Affinity for the Aryl Hydrocarbon Receptor

2019 ◽  
Vol 171 (2) ◽  
pp. 443-462 ◽  
Author(s):  
Nettie van Meteren ◽  
Dominique Lagadic-Gossmann ◽  
Martine Chevanne ◽  
Isabelle Gallais ◽  
Dimitri Gobart ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factor ◽  
Polycyclic Aromatic Hydrocarbons ◽  
Cell Membrane ◽  
Aryl Hydrocarbon Receptor ◽  
Extracellular Vesicles ◽  
Aromatic Hydrocarbons ◽  
Aryl Hydrocarbon ◽  
Polycyclic Aromatic ◽  
Cell Membrane Fluidity

Abstract Extracellular vesicles (EVs) are membrane-enclosed nanostructures released by cells into the extracellular environment. As major actors of physiological intercellular communication, they have been shown to be pathogenic mediators of several liver diseases. Extracellular vesicles also appear to be potential actors of drug-induced liver injury but nothing is known concerning environmental pollutants. We aimed to study the impact of polycyclic aromatic hydrocarbons (PAHs), major contaminants, on hepatocyte-derived EV production, with a special focus on hepatocyte death. Three PAHs were selected, based on their presence in food and their affinity for the aryl hydrocarbon receptor (AhR): benzo[a]pyrene (BP), dibenzo[a,h]anthracene (DBA), and pyrene (PYR). Treatment of primary rat and WIF-B9 hepatocytes by all 3 PAHs increased the release of EVs, mainly comprised of exosomes, in parallel with modifying exosome protein marker expression and inducing apoptosis. Moreover, PAH treatment of rodents for 3 months also led to increased EV levels in plasma. The EV release involved CYP metabolism and the activation of the transcription factor, the AhR, for BP and DBA and another transcription factor, the constitutive androstane receptor, for PYR. Furthermore, all PAHs increased cholesterol levels in EVs but only BP and DBA were able to reduce the cholesterol content of total cell membranes. All cholesterol changes very likely participated in the increase in EV release and cell death. Finally, we studied changes in cell membrane fluidity caused by BP and DBA due to cholesterol depletion. Our data showed increased cell membrane fluidity, which contributed to hepatocyte EV release and cell death.

scholarly journals Tryptophan Metabolism Activates Aryl Hydrocarbon Receptor-Mediated Pathway To Promote HIV-1 Infection and Reactivation

mBio ◽  
2019 ◽  
Vol 10 (6) ◽  
Author(s):  
Yan-Heng Zhou ◽  
Li Sun ◽  
Jun Chen ◽  
Wei-Wei Sun ◽  
Li Ma ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Metabolic Pathways ◽  
Nuclear Translocation ◽  
Underlying Mechanism ◽  
Hiv Pathogenesis ◽  
Downstream Target ◽  
Potential Target ◽  
Aryl Hydrocarbon ◽  
Hiv 1

ABSTRACT Multiple cellular metabolic pathways are altered by HIV-1 infection, with an impact on immune activation, inflammation, and acquisition of non-AIDS comorbid diseases. The dysfunction of tryptophan (Trp) metabolism has been observed clinically in association with accelerated HIV-1 pathogenesis, but the underlying mechanism remains unknown. In this study, we demonstrated that the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, is activated by Trp metabolites to promote HIV-1 infection and reactivation. AHR directly binds to the HIV-1 5′ long terminal repeat (5′-LTR) at the molecular level to activate viral transcription and infection, and AHR activation by Trp metabolites increases its nuclear translocation and association with the HIV 5′-LTR; moreover, the binding of AHR with HIV-1 Tat facilitates the recruitment of positive transcription factors to viral promoters. These findings not only elucidate a previously unappreciated mechanism through which cellular Trp metabolites affect HIV pathogenesis but also suggest that a downstream target AHR may be a potential target for modulating HIV-1 infection. IMPORTANCE Cellular metabolic pathways that are altered by HIV-1 infection may accelerate disease progression. Dysfunction in tryptophan (Trp) metabolism has been observed clinically in association with accelerated HIV-1 pathogenesis, but the mechanism responsible was not known. This study demonstrates that Trp metabolites augment the activation of aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, to promote HIV-1 infection and transcription. These findings not only elucidate a previously unappreciated mechanism through which cellular Trp metabolites affect HIV pathogenesis but also suggest that a downstream target AHR may be a potential target for modulating HIV-1 infection.

Serum from Methimazole-Treated Patients Induces Activation of Aryl Hydrocarbon Receptor, a Transcription Factor That Binds to Dioxin-Response Elements

Thyroid ◽  
2012 ◽  
Vol 22 (8) ◽  
pp. 769-777 ◽  
Author(s):  
Toshio Ishikawa ◽  
Hiroko Okinaga ◽  
Satoshi Takahashi ◽  
Maiko Numakura ◽  
Yamato Mashimo ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Response Elements ◽  
Aryl Hydrocarbon

Expression of the aryl hydrocarbon receptor/transcription factor (AhR) and AhR-regulated CYP1

2000 ◽  
Vol 63 (2) ◽  
pp. 117-131 ◽  
Author(s):  
Anthony F. Trombino ◽  
Richard I. Near ◽  
Raymond A. Matulka ◽  
Shi Yang ◽  
Laurie J. Hafer ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon

Regulation of PreB Cell Apoptosis by Aryl Hydrocarbon Receptor/Transcription Factor‐Expressing Stromal/Adherent Cells

1999 ◽  
Vol 221 (3) ◽  
pp. 242-252 ◽  
Author(s):  
Richard I. Near ◽  
Raymond A. Matulka ◽  
Koren K. Mann ◽  
Shaila U. Gogate ◽  
Anthony F. Trombino ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Cell Apoptosis ◽  
Adherent Cells ◽  
Aryl Hydrocarbon
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