Literature DB >> 9864300

Lipopolysaccharide activation of murine splenocytes and splenic B cells increased the expression of aryl hydrocarbon receptor and aryl hydrocarbon receptor nuclear translocator.

R S Marcus1, M P Holsapple, N E Kaminski.   

Abstract

These studies characterized the profile of AhR and ARNT expression in primary splenocytes and purified splenic B cells after cellular activation with lipopolysaccharide (LPS). LPS treatment of mouse splenocytes markedly increased the magnitude of both AhR and ARNT steady state mRNA expression. AhR mRNA expression peaked at 8 hr post-LPS activation and was increased by approximately 5-fold compared with freshly isolated splenocytes (i.e., time 0). ARNT mRNA expression began to increase at 8 hr postactivation, peaked at approximately 48 hr and was increased by approximately 4-fold when compared with nonactivated splenocytes at time 0. Western blotting also demonstrated an increase in the relative magnitude of both the AhR and ARNT proteins in LPS activated splenocytes. Likewise, the presence of the AhR, ARNT and cytochrome P450IA1 (CYP1A1) proteins were also detected in purified primary splenic B cells, and the magnitude of protein expression was enhanced in LPS activated splenic B cells at 12 and 24 hr relative to time matched controls for each of these proteins. In summary, these findings suggest that on LPS activation the magnitude of AhR and ARNT mRNA and protein increases in both splenocytes and purified primary splenic B cells. Moreover, because the increase in the relative magnitude of CYP1A1 protein in response to LPS occurred in the absence of exogenous AhR ligand, these results suggest that B-cell activation is sufficient to induce AhR nuclear translocation and binding to dioxin-responsive elements in the promoter region of AhR-responsive genes.

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Year:  1998        PMID: 9864300

Source DB:  PubMed          Journal:  J Pharmacol Exp Ther        ISSN: 0022-3565            Impact factor:   4.030


  12 in total

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Authors:  Michael A Wheeler; Veit Rothhammer; Francisco J Quintana
Journal:  J Biol Chem       Date:  2017-06-14       Impact factor: 5.157

2.  An integrated genomic analysis of aryl hydrocarbon receptor-mediated inhibition of B-cell differentiation.

Authors:  K Nadira De Abrew; Norbert E Kaminski; Russell S Thomas
Journal:  Toxicol Sci       Date:  2010-09-06       Impact factor: 4.849

3.  The AhR and NF-κB/Rel Proteins Mediate the Inhibitory Effect of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin on the 3' Immunoglobulin Heavy Chain Regulatory Region.

Authors:  Richard L Salisbury; Courtney E W Sulentic
Journal:  Toxicol Sci       Date:  2015-09-16       Impact factor: 4.849

Review 4.  The long winding road toward understanding the molecular mechanisms for B-cell suppression by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Authors:  Courtney E W Sulentic; Norbert E Kaminski
Journal:  Toxicol Sci       Date:  2010-10-15       Impact factor: 4.849

5.  2,3,7,8-tetrachlorodibenzo-p-dioxin induces transcriptional activity of the human polymorphic hs1,2 enhancer of the 3'Igh regulatory region.

Authors:  Tharu M Fernando; Sharon D Ochs; Jing Liu; Ruth C Chambers-Turner; Courtney E W Sulentic
Journal:  J Immunol       Date:  2012-02-22       Impact factor: 5.422

6.  A bistable switch underlying B-cell differentiation and its disruption by the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Authors:  Sudin Bhattacharya; Rory B Conolly; Norbert E Kaminski; Russell S Thomas; Melvin E Andersen; Qiang Zhang
Journal:  Toxicol Sci       Date:  2010-02-01       Impact factor: 4.849

7.  Focused examination of the intestinal lamina propria yields greater molecular insight into mechanisms underlying SIV induced immune dysfunction.

Authors:  Mahesh Mohan; Deepak Kaushal; Pyone P Aye; Xavier Alvarez; Ronald S Veazey; Andrew A Lackner
Journal:  PLoS One       Date:  2012-04-12       Impact factor: 3.240

8.  Role of the Arylhydrocarbon Receptor (AhR) in the Pathology of Asthma and COPD.

Authors:  Takahito Chiba; Junichi Chihara; Masutaka Furue
Journal:  J Allergy (Cairo)       Date:  2012-01-29

9.  Aryl hydrocarbon receptor is required for optimal B-cell proliferation.

Authors:  Matteo Villa; Manolis Gialitakis; Mauro Tolaini; Helena Ahlfors; Colin J Henderson; C Roland Wolf; Robert Brink; Brigitta Stockinger
Journal:  EMBO J       Date:  2016-11-14       Impact factor: 11.598

Review 10.  The role of the aryl hydrocarbon receptor in normal and malignant B cell development.

Authors:  David H Sherr; Stefano Monti
Journal:  Semin Immunopathol       Date:  2013-08-13       Impact factor: 9.623

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