Evidence map›Paper›PMID 21943234›Full record

ArticleStem cells and development2012

DEK regulates hematopoietic stem engraftment and progenitor cell proliferation.

Hal E Broxmeyer, Ferdinand Kappes, Nirit Mor-Vaknin, Maureen Legendre, John Kinzfogl, Scott Cooper, Giao Hangoc, David M Markovitz

Open access · greenAbstract read
In one paragraph

Article in Stem cells and development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 38 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

8 authors at 2 institutions in 2 countries.

Hal E BroxmeyerDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana 46202-5181, USA. hbroxmey@iupui.edu
Ferdinand Kappes
Nirit Mor-Vaknin
Maureen Legendre
John Kinzfogl
Scott Cooper
Giao Hangoc
David M Markovitz
University of Michigan · USUniversity School · US

Funding

REGULATION OF HEMATOPOIETIC CELL PRODUCTIONT32DK007519 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 1986 to 2020
$7.1M
MECHANISMS OF SYNERGISTIC REGULATION OF STEM/PROGENITORSR01HL056416 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BROXMEYER, HAL E. · 1996 to 2017
$6.0M
DEK and TNF inhibitors in juvenile arthritisR01AI087128 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MARKOVITZ, DAVID MICHAEL · 2009 to 2012
$1.5M
Regulation of Vascular Smooth Muscle ContractingR01HL067284 · NHLBI · UNIVERSITY OF KENTUCKY · PI GONG, MING C · 2002 to 2005
$1.0M
The Role of DEK in the Development of ArthritisK01AR055620 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOR-VAKNIN, NIRIT · 2009 to 2013
$541k
The Role of DEK in the Development of ArthritisR03AR056748 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOR-VAKNIN, NIRIT · 2009 to 2011
$206k
NHLBI NIH HHS HL07910NHLBI NIH HHS R01 HL056416NHLBI NIH HHS R01 HL067284NIAID NIH HHS R01 AI087128NIAMS NIH HHS K01 AR055620NIAMS NIH HHS R03 AR056748NIDDK NIH HHS DK07519
6 · The paper itself

Abstract

DEK is a biochemically distinct protein that is generally found in the nucleus, where it is vital to global heterochromatin integrity. However, DEK is also secreted by cells (eg, macrophages) and influences other adjacent cells (eg, acts as a chemoattractant for certain mature blood cells). We hypothesized that DEK may modulate functions of hematopoietic stem (HSCs) and progenitor (HPCs) cells. C57Bl/6 mice were used to demonstrate that absolute numbers and cycling status of HPCs (colony forming unit-granulocyte macrophage [CFU-GM], burst forming unit-erythroid [BFU-E], and colony forming unit-granulocyte erythroid macrophage megakaryocyte [CFU-GEMM]) in bone marrow (BM) and spleen were significantly enhanced in DEK -/- as compared with wild-type (WT) control mice. Moreover, purified recombinant DEK protein inhibited colony formation in vitro by CFU-GM, BFU-E, and CFU-GEMM from WT BM cells and human cord blood (CB) cells in a dose-dependent fashion, demonstrating that DEK plays a negative role in HPC proliferation in vitro and in vivo. Suppression was direct acting as determined by inhibition of proliferation of single isolated CD34(+) CB cells in vitro. In contrast, DEK -/- BM cells significantly demonstrated reduced long term competitive and secondary mouse repopulating HSC capacity compared with WT BM cells, demonstrating that DEK positively regulates engrafting capability of self-renewing HSCs. This demonstrates that DEK has potent effects on HSCs, HPCs, and hematopoiesis, information of biological and potential clinical interest.

Indexed as

Graft SurvivalHematopoietic Stem Cell TransplantationAnimalsCell ProliferationChromosomal Proteins, Non-HistoneDNA-Binding ProteinsHematopoietic Stem CellsHumansMiceMice, KnockoutOncogene ProteinsPoly-ADP-Ribose Binding ProteinsTransplantation, HeterologousTransplantation, HomologousChromosomal Proteins, Non-HistoneDEK protein, humanDEK protein, mouseDNA-Binding ProteinsOncogene ProteinsPoly-ADP-Ribose Binding Proteins

Identifiers

PMID21943234
PMCPMC3359622
OpenAlexW2055090398

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.