Evidence map›Paper›PMID 27366154›Full record

ArticleStem cells international2016

Aryl Hydrocarbon Receptor Deficiency in an Exon 3 Deletion Mouse Model Promotes Hematopoietic Stem Cell Proliferation and Impacts Endosteal Niche Cells.

Zeenath Unnisa, Kameshwar P Singh, Ellen C Henry, Catherine L Donegan, John A Bennett, Thomas A Gasiewicz

Open access · goldAbstract read
In one paragraph

Article in Stem cells international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 27 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Zeenath UnnisaDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Kameshwar P SinghDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Ellen C HenryDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Catherine L DoneganDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
John A BennettDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Thomas A GasiewiczDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
University of Rochester Medical Center · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Sally W Thurston · 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
Signaling Pathway in Ah Receptor-Dependent Control of Hematopoietic Stem CellsR01ES023068 · NIEHS · UNIVERSITY OF ROCHESTER · PI SINGH, KAMESHWAR P · 2013 to 2017
$1.7M
NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R01 ES004862NIEHS NIH HHS R01 ES023068NIEHS NIH HHS T32 ES007026
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor belonging to the Per-Arnt-Sim (PAS) family of proteins. The AHR is involved in hematopoietic stem cell (HSC) functions including self-renewal, proliferation, quiescence, and differentiation. We hypothesize that AHR impacts HSC functions by influencing genes that have roles in HSC maintenance and function and that this may occur through regulation of bone marrow (BM) niche cells. We examined BM and niche cells harvested from 8-week-old AHR null-allele (KO) mice in which exon 3 was deleted in the Ahr gene and compared these data to cells from B6 control mice; young and old (10 months) animals were also compared. We report changes in HSCs and peripheral blood cells in mice lacking AHR. Serial transplantation assays revealed a significant increase in long term HSCs. There was a significant increase in mesenchymal stem cells constituting the endosteal BM niche. Gene expression analyses of HSCs revealed an increase in expression of genes involved in proliferation and maintenance of quiescence. Our studies infer that loss of AHR results in increased proliferation and self-renewal of long term HSCs, in part, by influencing the microenvironment in the niche regulating the balance between quiescence and proliferation in HSCs.

Identifiers

PMID27366154
PMCPMC4913018
OpenAlexW2406358370

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.