Evidence map›Paper›PMID 24590069›Full record

ArticleNature2014

Foxc1 is a critical regulator of haematopoietic stem/progenitor cell niche formation.

Yoshiki Omatsu, Masanari Seike, Tatsuki Sugiyama, Tsutomu Kume, Takashi Nagasawa

Abstract read
PubMed Publisher
In one paragraph

Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed
13.9field-weighted citation impact, top 1% 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

151 citing papers in PubMed, 260 citations in OpenAlex.

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  13. The RANK/RANKL axis controls vascular dynamics in the bone marrow.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  20. Hematopoietic stem cell metabolism within the bone marrow niche - insights and opportunities.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review

91 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 at 3 institutions in 2 countries.

Yoshiki Omatsu1] Department of Immunobiology and Hematology, Institute for Frontier Medical Sciences, Kyoto University, Japan [2] Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
Masanari Seike1] Department of Immunobiology and Hematology, Institute for Frontier Medical Sciences, Kyoto University, Japan [2] Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
Tatsuki Sugiyama1] Department of Immunobiology and Hematology, Institute for Frontier Medical Sciences, Kyoto University, Japan [2] Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
Tsutomu KumeFeinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.
Takashi Nagasawa1] Department of Immunobiology and Hematology, Institute for Frontier Medical Sciences, Kyoto University, Japan [2] Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
Kyoto University · JPJapan Science and Technology Agency · JPNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Haematopoietic stem and progenitor cells are maintained by special microenvironments known as niches in bone marrow. Many studies have identified diverse candidate cells that constitute niches for haematopoietic stem cells in the marrow, including osteoblasts, endothelial cells, Schwann cells, α-smooth muscle actin-expressing macrophages and mesenchymal progenitors such as CXC chemokine ligand (CXCL)12-abundant reticular (CAR) cells, stem cell factor-expressing cells, nestin-expressing cells and platelet-derived growth factor receptor-α (PDGFR-α)(+)Sca-1(+)CD45(-)Ter119(-) (PαS) cells. However, the molecular basis of the formation of the niches remains unclear. Here we find that the transcription factor Foxc1 is preferentially expressed in the adipo-osteogenic progenitor CAR cells essential for haematopoietic stem and progenitor cell maintenance in vivo in the developing and adult bone marrow. When Foxc1 was deleted in all marrow mesenchymal cells or CAR cells, from embryogenesis onwards, osteoblasts appeared normal, but haematopoietic stem and progenitor cells were markedly reduced and marrow cavities were occupied by adipocytes (yellow adipose marrow) with reduced CAR cells. Inducible deletion of Foxc1 in adult mice depleted haematopoietic stem and progenitor cells and reduced CXCL12 and stem cell factor expression in CAR cells but did not induce a change to yellow marrow. These data suggest a role for Foxc1 in inhibiting adipogenic processes in CAR progenitors. Foxc1 might also promote CAR cell development, upregulating CXCL12 and stem cell factor expression. This study identifies Foxc1 as a specific transcriptional regulator essential for development and maintenance of the mesenchymal niches for haematopoietic stem and progenitor cells.

Indexed as

AdipocytesAnimalsBone Marrow CellsCell CountCell DifferentiationChemokine CXCL12Embryonic DevelopmentForkhead Transcription FactorsHematopoietic Stem CellsMesenchymal Stem CellsMiceOsteoblastsStem Cell FactorStem Cell NicheChemokine CXCL12Forkhead Transcription FactorsFoxc1 protein, mouseStem Cell Factor

Identifiers

PMID24590069
OpenAlexW1980587308

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.