Evidence map›Paper›PMID 10377195›Full record

ArticleThe Journal of experimental medicine1999

Dominant myelopoietic effector functions mediated by chemokine receptor CCR1.

H E Broxmeyer, S Cooper, G Hangoc, J L Gao, P M Murphy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 111 citations in OpenAlex.

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  15. Beta-Chemokine CCL15 Affects the Adhesion and Migration of Hematopoietic Progenitor Cells.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2015
    Article
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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

5 authors at 3 institutions in 1 country.

H E BroxmeyerDepartment of Microbiology/Immunology, the Department of Medicine, and the Walther Oncology Center, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA. hbroxmey@iupui.edu
S Cooper
G Hangoc
J L Gao
P M Murphy
National Institutes of Health · USWalther Cancer Foundation · USIndiana University – Purdue University Indianapolis · US

Funding

MOLECULAR ANALYSIS OF NEUTROPHIL ACTIVATION BY CHEMOATTRACTANTSZ01AI000615 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI MURPHY, PHILIP · 1991 to 2008
$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
CHEMOKINES/CYTOKINES AND RECEPTORS IN STEM CELL HOMINGR01DK053674 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BROXMEYER, HAL E. · 1997 to 2005
$1.6M
NHLBI NIH HHS R01 HL056416NHLBI NIH HHS R01 HL56416NIDDK NIH HHS R01 DK053674NIDDK NIH HHS R01 DK53674
6 · The paper itself

Abstract

Macrophage inflammatory protein (MIP)-1alpha, a CC chemokine, enhances proliferation of mature subsets of myeloid progenitor cells (MPCs), suppresses proliferation of immature MPCs, and mobilizes mature and immature MPCs to the blood. MIP-1alpha binds at least three chemokine receptors. To determine if CCR1 was dominantly mediating the above activities of MIP-1alpha, CCR1-deficient (-/-) mice, produced by targeted gene disruption, were used. MIP-1alpha enhanced colony formation of marrow granulocyte/macrophage colony-forming units (CFU-GM), responsive to stimulation by granulocyte/macrophage colony-stimulating factor (GM-CSF), and CFU-M, responsive to stimulation by M-CSF, from littermate control CCR1(+/+) but not CCR1(-/-) mice. Moreover, MIP-1alpha did not mobilize MPCs to the blood or synergize with G-CSF in this effect in CCR1(-/-) mice. However, CCR1(-/-) mice were increased in sensitivity to MPC mobilizing effects of G-CSF. Multi-growth factor-stimulated MPCs in CCR1(-/-) and CCR1(+/+) marrow were equally sensitive to inhibition by MIP-1alpha. These results implicate CCR1 as a dominant receptor for MIP-1alpha enhancement of proliferation of lineage-committed MPCs and for mobilization of MPCs to the blood. CCR1 is not a dominant receptor for MIP-1alpha suppression of MPC proliferation, but it does negatively impact G-CSF-induced MPC mobilization.

Indexed as

AnimalsCell DivisionChemokine CCL3Chemokine CCL4ChemokinesColony-Forming Units AssayErythroid Precursor CellsGranulocyte-Macrophage Colony-Stimulating FactorHumansLeukopoiesisMacrophage Inflammatory ProteinsMiceMice, KnockoutReceptors, CCR1Receptors, ChemokineStem CellsCCR1 protein, humanCcr1 protein, mouseChemokine CCL3Chemokine CCL4ChemokinesGranulocyte-Macrophage Colony-Stimulating FactorMacrophage Inflammatory ProteinsReceptors, CCR1Receptors, Chemokine

Identifiers

PMID10377195
PMCPMC2192966
OpenAlexW2126231800

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.