Evidence map›Paper›PMID 29581184›Full record

ArticleMolecular and cellular biology2018

Loss of the Hematopoietic Stem Cell Factor GATA2 in the Osteogenic Lineage Impairs Trabecularization and Mechanical Strength of Bone.

Alexander Tolkachov, Cornelius Fischer, Thomas H Ambrosi, Melissa Bothe, Chung-Ting Han, Matthias Muenzner, Susanne Mathia, Marjo Salminen, Georg Seifert, Mario Thiele and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  7. Exploring the Interplay between Bone Marrow Stem Cells and Obesity.International journal of molecular sciences · 2024
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  16. Obesity-Induced Changes in Bone Marrow Homeostasis.Frontiers in endocrinology · 2020
    Review
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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

15 authors at 8 institutions in 2 countries.

Alexander TolkachovCharité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pharmacology, Berlin, Germany.
Cornelius FischerLaboratory of Functional Genomics, Nutrigenomics and Systems Biology, BIMSB and BIH Genomics Platforms, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Thomas H AmbrosiResearch Group Adipocyte Development, German Institute of Human Nutrition (DlfE), Potsdam-Rehbrucke, Nuthetal, Germany.
Melissa BotheMax Planck Institute for Molecular Genetics, Berlin, Germany.
Chung-Ting HanLaboratory of Functional Genomics, Nutrigenomics and Systems Biology, BIMSB and BIH Genomics Platforms, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Matthias MuenznerCharité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pharmacology, Berlin, Germany.
Susanne MathiaCharité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Nephrology and Renal Transplantation, Berlin, Germany.
Marjo SalminenDepartment of Veterinary Biosciences, University of Helsinki, Helsinki, Finland.
Georg SeifertCharité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Pediatric Oncology/Hematology, Otto Heubner Center for Pediatric and Adolescent Medicine, Berlin, Germany.
Mario ThieleCharité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Julius Wolff Institute and Berlin-Brandenburg School for Regenerative Therapies, Berlin, Germany.
Georg N DudaCharité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Julius Wolff Institute and Berlin-Brandenburg School for Regenerative Therapies, Berlin, Germany.
Sebastiaan H MeijsingMax Planck Institute for Molecular Genetics, Berlin, Germany.
Sascha SauerLaboratory of Functional Genomics, Nutrigenomics and Systems Biology, BIMSB and BIH Genomics Platforms, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Tim J SchulzResearch Group Adipocyte Development, German Institute of Human Nutrition (DlfE), Potsdam-Rehbrucke, Nuthetal, Germany.
Michael SchuppCharité-Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pharmacology, Berlin, Germany michael.schupp@charite.de.
Charité - Universitätsmedizin Berlin · DEMax Delbrück Center · DEBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DEMax Planck Institute for Molecular Genetics · DEDeutsches Diabetes-Zentrum e.V. · DEGerman Institute of Human Nutrition · DEHumboldt-Universität zu Berlin · DEUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor GATA2 is required for expansion and differentiation of hematopoietic stem cells (HSCs). In mesenchymal stem cells (MSCs), GATA2 blocks adipogenesis, but its biological relevance and underlying genomic events are unknown. We report a dual function of GATA2 in bone homeostasis. GATA2 in MSCs binds near genes involved in skeletal system development and colocalizes with motifs for FOX and HOX transcription factors, known regulators of skeletal development. Ectopic GATA2 blocks osteoblastogenesis by interfering with SMAD1/5/8 activation. MSC-specific deletion of GATA2 in mice increases the numbers and differentiation capacity of bone-derived precursors, resulting in elevated bone formation. Surprisingly, MSC-specific GATA2 deficiency impairs the trabecularization and mechanical strength of bone, involving reduced MSC expression of the osteoclast inhibitor osteoprotegerin and increased osteoclast numbers. Thus, GATA2 affects bone turnover via MSC-autonomous and indirect effects. By regulating bone trabecularization, GATA2 expression in the osteogenic lineage may contribute to the anatomical and cellular microenvironment of the HSC niche required for hematopoiesis.

Indexed as

3T3 CellsAnimalsBinding SitesBone and BonesBone Marrow CellsCell DifferentiationCell LineCellular MicroenvironmentFractures, BoneGATA2 DeficiencyGATA2 Transcription FactorGene Expression Regulation, DevelopmentalHematopoietic Stem CellsMaleMesenchymal Stem CellsMiceGata2 protein, mouseGATA2 Transcription FactorNuclear ProteinsSmad1 ProteinSmad1 protein, mouseSmad5 ProteinSmad5 protein, mouseSmad8 ProteinSmad9 protein, mouseTranscription FactorsZfpm1 protein, mousebonecell differentiationGATA2mesenchymal stem cellosteoblasttrabecularization

Identifiers

PMID29581184
PMCPMC5974429
OpenAlexW2790252984

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.