Evidence map›Paper›PMID 20185584›Full record

ArticleBlood2010

STAT3 controls the neutrophil migratory response to CXCR2 ligands by direct activation of G-CSF-induced CXCR2 expression and via modulation of CXCR2 signal transduction.

Hoainam Nguyen-Jackson, Athanasia D Panopoulos, Huiyuan Zhang, Haiyan S Li, Stephanie S Watowich

Abstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

83 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Neutrophils in cancer.Nature reviews. Cancer · 2026
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23 more citing papers are in PubMed but not listed here.

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.

Hoainam Nguyen-JacksonDepartment of Immunology and Center for Cancer Immunology Research, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA.
Athanasia D Panopoulos
Huiyuan Zhang
Haiyan S Li
Stephanie S Watowich

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Training Program in Cancer ImmunobiologyT32CA009598 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ALLISON, JAMES P · 1988 to 2014
$4.9M
Cytokine Regulation of Dendritic Cell DevelopmentR21AI073587 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WATOWICH, STEPHANIE S · 2007 to 2008
$409k
NCI NIH HHS P30 CA016672NCI NIH HHS T32 CA009598NCI NIH HHS T32-CA-09598-16NIAID NIH HHS AI073587NIAID NIH HHS R21 AI073587
6 · The paper itself

Abstract

Neutrophil mobilization, the release of neutrophils from the bone marrow reserve into circulating blood, is important to increase peripheral neutrophil amounts during bacterial infections. Granulocyte colony-stimulating factor (G-CSF) and chemokines, such as macrophage-inflammatory protein-2 (MIP-2; CXCL2), can induce neutrophil mobilization, but the mechanism(s) they use remain unclear. Signal transducers and activator of transcription 3 (STAT3) is the principal intracellular signaling molecule activated upon G-CSF ligation of its receptor. Using a murine model with conditional STAT3 deletion in bone marrow, we demonstrated previously that STAT3 regulates acute G-CSF-responsive neutrophil mobilization and MIP-2-dependent neutrophil chemotaxis. In this study, we show STAT3 is also necessary for MIP-2-elicited neutrophil mobilization. STAT3 appears to function by controlling extracellular signal-regulated kinase (ERK) activation, which is important for MIP-2-mediated chemotaxis. In addition, we demonstrate that G-CSF stimulates the expression of the MIP-2 receptor via STAT3-dependent transcriptional activation of Il8rb. G-CSF treatment also induces STAT3-dependent changes in bone marrow chemokine expression levels which may further affect neutrophil retention and release. Taken together, our study demonstrates that STAT3 regulates multiple aspects of chemokine and chemokine receptor expression and function within the bone marrow, indicating a central role in the neutrophil mobilization response.

Indexed as

AnimalsCell SeparationChemokine CXCL2Chemotaxis, LeukocyteElectrophoretic Mobility Shift AssayFlow CytometryGene ExpressionGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorImmunoblottingImmunoprecipitationMiceMice, TransgenicNeutrophilsReceptors, Interleukin-8Reverse Transcriptase Polymerase Chain ReactionChemokine CXCL2Cxcl2 protein, mouseGranulocyte-Macrophage Colony-Stimulating FactorReceptors, Interleukin-8Stat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID20185584
PMCPMC2858484

What OpenQuestion holds

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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.