Evidence map›Paper›PMID 24152593›Full record

ArticleCell adhesion & migration

BIGH3 modulates adhesion and migration of hematopoietic stem and progenitor cells.

Sofieke E Klamer, Carlijn G M Kuijk, Peter L Hordijk, C Ellen van der Schoot, Marieke von Lindern, Paula B van Hennik, Carlijn Voermans

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In one paragraph

Article in Cell adhesion & migration. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Biomarkers of tumor invasiveness in proteomics (Review).International journal of oncology · 2020
    Pooled it
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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

7 authors at 3 institutions in 1 country.

Sofieke E KlamerDepartment of Hematopoiesis; Sanquin Research and Landsteiner Laboratory; Academic Medical Centre; University of Amsterdam; Amsterdam, the Netherlands.
Carlijn G M KuijkDepartment of Hematopoiesis; Sanquin Research and Landsteiner Laboratory; Academic Medical Centre; University of Amsterdam; Amsterdam, the Netherlands.
Peter L HordijkDepartment of Molecular Cell Biology; Sanquin Research and Landsteiner Laboratory; Academic Medical Centre; University of Amsterdam; Amsterdam, the Netherlands.
C Ellen van der SchootDepartment of Experimental Immunohematology; Sanquin Research and Landsteiner Laboratory; Academic Medical Centre; University of Amsterdam; Amsterdam, the Netherlands; Department of Hematology; Academic Medical Centre; Amsterdam, the Netherlands.
Marieke von LindernDepartment of Hematopoiesis; Sanquin Research and Landsteiner Laboratory; Academic Medical Centre; University of Amsterdam; Amsterdam, the Netherlands.
Paula B van HennikDepartment of Hematopoiesis; Sanquin Research and Landsteiner Laboratory; Academic Medical Centre; University of Amsterdam; Amsterdam, the Netherlands.
Carlijn VoermansDepartment of Hematopoiesis; Sanquin Research and Landsteiner Laboratory; Academic Medical Centre; University of Amsterdam; Amsterdam, the Netherlands.
Academic Medical Center · NLUniversity of Amsterdam · NLSanquin · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell adhesion and migration are important determinants of homing and development of hematopoietic stem and progenitor cells (HSPCs) in bone marrow (BM) niches. The extracellular matrix protein transforming growth factor-β (TGF-β) inducible gene H3 (BIGH3) is involved in adhesion and migration, although the effect of BIGH3 is highly cell type-dependent. BIGH3 is abundantly expressed by mesenchymal stromal cells, while its expression in HSPCs is relatively low unless induced by certain BM stressors. Here, we set out to determine how BIGH3 modulates HSPC adhesion and migration. We show that primary HSPCs adhere to BIGH3-coated substrates, which is, in part, integrin-dependent. Overexpression of BIGH3 in HSPCs and HL60 cells reduced the adhesion to the substrate fibronectin in adhesion assays, which was even more profound in electrical cell-substrate impedance sensing (ECIS) assays. Accordingly, the CXCL12 induced migration over fibronectin-coated surface was reduced in BIGH3-expressing HSPCs. The integrin expression profile of HSPCs was not altered upon BIGH3 expression. Although expression of BIGH3 did not alter actin polymerization in response to CXCL12, it inhibited the PMA-induced activation of the small GTPase RAC1 as well as the phosphorylation and activation of extracellular-regulated kinases (ERKs). Reduced activation of ERK and RAC1 may be responsible for the inhibition of cell adhesion and migration by BIGH3 in HSPCs. Induced BIGH3 expression upon BM stress may contribute to the regulation of BM homeostasis.

Indexed as

betaIG-H3 ProteinBone Marrow CellsCell AdhesionCell MovementChemokine CXCL12Electric ImpedanceExtracellular Matrix ProteinsFibronectinsHematopoietic Stem CellsHumansIntegrinsStem CellsTransforming Growth Factor betabetaIG-H3 ProteinChemokine CXCL12Extracellular Matrix ProteinsFibronectinsIntegrinsTransforming Growth Factor betaadhesionBIGH3ECISECMERKhematopoiesisHSPCintegrinsmigrationRAC1

Identifiers

PMID24152593
PMCPMC3903689
OpenAlexW2074288155

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.