Evidence map›Paper›PMID 28673932›Full record

ArticleThe EMBO journal2017

Integrin αvβ3 enhances the suppressive effect of interferon-γ on hematopoietic stem cells.

Terumasa Umemoto, Yu Matsuzaki, Yoshiko Shiratsuchi, Michihiro Hashimoto, Takayuki Yoshimoto, Ayako Nakamura-Ishizu, Brian Petrich, Masayuki Yamato, Toshio Suda

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  6. Identification and Characterization of CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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  19. αvβ3-integrin regulates PD-L1 expression and is involved in cancer immune evasion.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  20. CaThe Journal of experimental medicine · 2018
    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

9 authors at 5 institutions in 3 countries.

Terumasa UmemotoInternational Research Center for Medical Science, Kumamoto University, Kumamoto, Japan umemoto@kumamoto-u.ac.jp csits@nus.edu.sg.ORCID 0000-0003-0423-9003
Yu MatsuzakiInternational Research Center for Medical Science, Kumamoto University, Kumamoto, Japan.
Yoshiko ShiratsuchiInstitute of Advanced Medical Bioscience and Engineering, Tokyo Women's Medical University, Tokyo, Japan.
Michihiro HashimotoInternational Research Center for Medical Science, Kumamoto University, Kumamoto, Japan.
Takayuki YoshimotoDepartment of Immunoregulation, Institute of Medical Science, Tokyo Medical University, Tokyo, Japan.
Ayako Nakamura-IshizuCancer Science Institute of Singapore, National University of Singapore, Singapore City, Singapore.
Brian PetrichDepartment of Pediatrics and Aflac Cancer and Blood Disorders Center, Emory University School of Medicine, Atlanta, GA, USA.
Masayuki YamatoInstitute of Advanced Medical Bioscience and Engineering, Tokyo Women's Medical University, Tokyo, Japan.
Toshio SudaInternational Research Center for Medical Science, Kumamoto University, Kumamoto, Japan umemoto@kumamoto-u.ac.jp csits@nus.edu.sg.ORCID 0000-0001-7540-1771
Kumamoto Medical Center · JPNational University of Singapore · SGTokyo Women's Medical University · JPEmory University · USTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematopoietic homeostasis depends on the maintenance of hematopoietic stem cells (HSCs), which are regulated within a specialized bone marrow (BM) niche. When HSC sense external stimuli, their adhesion status may be critical for determining HSC cell fate. The cell surface molecule, integrin αvβ3, is activated through HSC adhesion to extracellular matrix and niche cells. Integrin β3 signaling maintains HSCs within the niche. Here, we showed the synergistic negative regulation of the pro-inflammatory cytokine interferon-γ (IFNγ) and β3 integrin signaling in murine HSC function by a novel definitive phenotyping of HSCs. Integrin αvβ3 suppressed HSC function in the presence of IFNγ and impaired integrin β3 signaling mitigated IFNγ-dependent negative action on HSCs. During IFNγ stimulation, integrin β3 signaling enhanced STAT1-mediated gene expression via serine phosphorylation. These findings show that integrin β3 signaling intensifies the suppressive effect of IFNγ on HSCs, which indicates that cell adhesion via integrin αvβ3 within the BM niche acts as a context-dependent signal modulator to regulate the HSC function under both steady-state and inflammatory conditions.

Indexed as

Cell ProliferationAnimalsGene Expression RegulationHematopoietic Stem CellsIntegrin alphaVbeta3Interferon-gammaMicePhosphorylationProtein Processing, Post-TranslationalSignal TransductionSTAT1 Transcription FactorIFNG protein, mouseIntegrin alphaVbeta3Interferon-gammaStat1 protein, mouseSTAT1 Transcription Factorhematopoietic stem cellsIFNγintegrin αvβ3STAT1

Identifiers

PMID28673932
PMCPMC5556268
OpenAlexW2727883962

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.