Enzyme induction and histopathology elucidate aryl hydrocarbon receptor-mediated versus non-aryl hydrocarbon receptor-mediated effects of Aroclor 1268 in American mink (Neovison vison)

2016 ◽  
Vol 35 (3) ◽  
pp. 619-634 ◽  
Author(s):  
William R. Folland ◽  
John L. Newsted ◽  
Scott D. Fitzgerald ◽  
Phyllis C. Fuchsman ◽  
Patrick W. Bradley ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Enzyme Induction ◽  
American Mink ◽  
Neovison Vison ◽  
Aryl Hydrocarbon ◽  
Mediated Effects ◽  
Aroclor 1268

scholarly journals Kynurenine Promotes RANKL-Induced Osteoclastogenesis In Vitro by Activating the Aryl Hydrocarbon Receptor Pathway

2020 ◽  
Vol 21 (21) ◽  
pp. 7931
Author(s):  
Nada H. Eisa ◽  
Sakamuri V. Reddy ◽  
Ahmed M. Elmansi ◽  
Galina Kondrikova ◽  
Dmitry Kondrikov ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Osteoclast Differentiation ◽  
Treatment Of Osteoporosis ◽  
Aryl Hydrocarbon ◽  
Mediated Effects ◽  
Receptor Activator ◽  
Raw 264.7 Macrophage Cells ◽  
Osteoclast Function

There is increasing evidence of the involvement of the tryptophan metabolite kynurenine (KYN) in disrupting osteogenesis and contributing to aging-related bone loss. Here, we show that KYN has an effect on bone resorption by increasing osteoclastogenesis. We have previously reported that in vivo treatment with KYN significantly increased osteoclast number lining bone surfaces. Here, we report the direct effect of KYN on receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastogenesis in Raw 264.7 macrophage cells, and we propose a potential mechanism for these KYN-mediated effects. We show that KYN/RANKL treatment results in enhancement of RANKL-induced osteoclast differentiation. KYN drives upregulation and activation of the key osteoclast transcription factors, c-fos and NFATc1 resulting in an increase in the number of multinucleated TRAP+ osteoclasts, and in hydroxyapatite bone resorptive activity. Mechanistically, the KYN receptor, aryl hydrocarbon receptor (AhR), plays an important role in the induction of osteoclastogenesis. We show that blocking AhR signaling using an AhR antagonist, or AhR siRNA, downregulates the KYN/RANKL-mediated increase in c-fos and NFATc1 and inhibits the formation of multinucleated TRAP + osteoclasts. Altogether, this work highlights that the novelty of the KYN and AhR pathways might have a potential role in helping to regulate osteoclast function with age and supports pursuing additional research to determine if they are potential therapeutic targets for the prevention or treatment of osteoporosis.

Aryl hydrocarbon receptor-mediated effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on glucose-stimulated insulin secretion in mice

2009 ◽  
Vol 29 (8) ◽  
pp. 689-694 ◽  
Author(s):  
Hisaka Kurita ◽  
Wataru Yoshioka ◽  
Noriko Nishimura ◽  
Naoto Kubota ◽  
Takashi Kadowaki ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon ◽  
Mediated Effects ◽  
Tetrachlorodibenzo P Dioxin ◽  
Glucose Stimulated Insulin Secretion

scholarly journals Assessment of Risks of Dioxins for Aryl Hydrocarbon Receptor-Mediated Effects in Polar Bear (Ursus maritimus) by in Vitro and in Silico Approaches

2019 ◽  
Vol 54 (3) ◽  
pp. 1770-1781 ◽  
Author(s):  
Ji-Hee Hwang ◽  
Kurunthachalam Kannan ◽  
Thomas J. Evans ◽  
Hisato Iwata ◽  
Eun-Young Kim
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
In Silico ◽  
Polar Bear ◽  
Ursus Maritimus ◽  
Aryl Hydrocarbon ◽  
Mediated Effects

Prediction of Aryl Hydrocarbon Receptor-Mediated Enzyme Induction of Drugs and Chemicals by mRNA Quantification

1998 ◽  
Vol 11 (12) ◽  
pp. 1447-1452 ◽  
Author(s):  
Roland Frötschl ◽  
Lubomir Chichmanov ◽  
Ullrich Kleeberg ◽  
Alfred G. Hildebrandt ◽  
Ivar Roots ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Enzyme Induction ◽  
Mrna Quantification ◽  
Aryl Hydrocarbon

Aryl Hydrocarbon Receptor-Mediated Effects of Chlorinated Polycyclic Aromatic Hydrocarbons

2007 ◽  
Vol 20 (9) ◽  
pp. 1237-1241 ◽  
Author(s):  
Takeshi Ohura ◽  
Maki Morita ◽  
Masakazu Makino ◽  
Takashi Amagai ◽  
Kayoko Shimoi
Keyword(s):  
Polycyclic Aromatic Hydrocarbons ◽  
Aryl Hydrocarbon Receptor ◽  
Aromatic Hydrocarbons ◽  
Aryl Hydrocarbon ◽  
Mediated Effects ◽  
Polycyclic Aromatic

Activation of the aryl hydrocarbon receptor promotes allograft-specific tolerance through direct and dendritic cell–mediated effects on regulatory T cells

Blood ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 1214-1222 ◽  
Author(s):  
Ehud Hauben ◽  
Silvia Gregori ◽  
Elena Draghici ◽  
Barbara Migliavacca ◽  
Stefano Olivieri ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Survival ◽  
Aryl Hydrocarbon Receptor ◽  
Cd4 T Cells ◽  
Aryl Hydrocarbon ◽  
Mediated Effects ◽  
Specific Tolerance

Abstract VAF347 is a low-molecular-weight compound, which activates the aryl hydrocarbon receptor (AhR). Herein, we report that oral administration of a water-soluble derivative of VAF347 (VAG539) promotes long-term graft acceptance and active tolerance in Balb/c mice that receive a transplant of MHC-mismatched pancreatic islet allografts. In vivo VAG539 treatment results in increased frequency of splenic CD4+ T cells expressing CD25 and Foxp3, markers associated with regulatory T (Tr) cells, and in vitro VAF347 treatment of splenic CD4+ T cells improved CD4+CD25+Foxp3+ T-cell survival. Interestingly, transfer of CD11c+ dendritic cells (DCs), but not of CD4+ T or CD19+ B cells, from VAG539-treated long-term tolerant hosts into mice that recently underwent transplantation resulted in donor (C57Bl/6)–specific graft acceptance and in a significantly higher frequency of splenic CD4+CD25+Foxp3+ Tr cells. Furthermore, the transfer of CD4+CD25+ T cells from these mice into mice that recently underwent transplantation promoted graft acceptance. Similarly, cell therapy with in vitro VAF347-treated bone marrow–derived mature DCs prevented islet graft rejection, and reduced OVA-specific T-cell responses in OVA-immunized mice. Collectively, our data indicate that AhR activation induces islet allograft–specific tolerance through direct as well as DC-mediated effects on Tr-cell survival and function.

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