Evidence map›Paper›PMID 21791576›Full record

ArticleMolecular pharmacology2011

Aryl hydrocarbon receptor activation in hematopoietic stem/progenitor cells alters cell function and pathway-specific gene modulation reflecting changes in cellular trafficking and migration.

Fanny L Casado, Kameshwar P Singh, Thomas A Gasiewicz

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Molecular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Aryl hydrocarbon receptor activation alters emergency hematopoiesis during influenza A virus infection.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Aryl Hydrocarbon Receptor: From Homeostasis to Tumor Progression.Frontiers in cell and developmental biology · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Fanny L CasadoDepartment of Environmental Medicine, University of Rochester, Rochester, NY, USA.
Kameshwar P Singh
Thomas A Gasiewicz
University of Rochester Medical Center · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
TCDD EFFECT ON T LYMPHOCYTE DIFFERENTIATIONR01ES004862 · NIEHS · UNIVERSITY OF ROCHESTER · PI LAWRENCE, B PAIGE · 1990 to 2020
$6.5M
BCL-2, ROS, AND CELL DEATH IN DEVELOPMENTAL TOXICITYR01ES007026 · NIEHS · UNIVERSITY OF WASHINGTON · PI MIRKES, PHILIP E · 1996 to 2002
$1.2M
A Role of the Ah Receptor in Hematopoiesis: Model CharacterizationR03ES016606 · NIEHS · UNIVERSITY OF ROCHESTER · PI GASIEWICZ, THOMAS A · 2009 to 2010
$153k
NIEHS NIH HHS ES01247NIEHS NIH HHS ES016606NIEHS NIH HHS ES04862NIEHS NIH HHS ES07026NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R01 ES004862NIEHS NIH HHS R01 ES007026NIEHS NIH HHS R03 ES016606NIEHS NIH HHS T32 ES007026
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a transcription factor belonging to the Per-ARNT-Sim family of proteins. These proteins sense molecules and stimuli from the cellular/tissue environment and initiate signaling cascades to elicit appropriate cellular responses. Recent literature reports suggest an important function of AhR in hematopoietic stem cell (HSC) biology. However, the molecular mechanisms by which AhR signaling regulates HSC functions are unknown. In previous studies, we and others reported that treatment of mice with the AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) compromises the competitive reconstitution of bone marrow (BM) cells into irradiated host animals. Additional studies indicated a requirement for AhR in hematopoietic cells and not marrow microenvironment cells. In this study, we tested the hypothesis that TCDD-mediated phenotypic and functional changes of HSCs are a result of changes in gene expression that disrupt stem cell numbers and/or their migration. TCDD treatment to mice increased the numbers of phenotypically defined HSCs in BM. These cells showed compromised migration to the BM in vivo and to the chemokine CXCL12 in vitro, as well as increased expression of the leukemia-associated receptors CD184 (CXCR4) and CD44. Gene expression profiles at 6 and 12 h after exposure were consistent with the phenotypic and functional changes observed. The expressions of Scin, Nqo1, Flnb, Mmp8, Ilf9, and Slamf7 were consistently altered. TCDD also disrupted expression of other genes involved in hematological system development and function including Fos, JunB, Egr1, Ptgs2 (Cox2), and Cxcl2. These data support a molecular mechanism for an AhR ligand to disrupt the homeostatic cell signaling of HSCs that may promote altered HSC function.

Indexed as

AnimalsBone Marrow TransplantationCell MovementFemaleHematopoietic Stem CellsMiceMice, Inbred C57BLProtein TransportReceptors, Aryl HydrocarbonSignal TransductionStem CellsReceptors, Aryl Hydrocarbon

Identifiers

PMID21791576
PMCPMC3187533
OpenAlexW2150992270

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.