Evidence map›Paper›PMID 27777239›Full record

ArticleBlood2016

TGF-β inhibitors stimulate red blood cell production by enhancing self-renewal of BFU-E erythroid progenitors.

Xiaofei Gao, Hsiang-Ying Lee, Edroaldo Lummertz da Rocha, Cheng Zhang, Yi-Fen Lu, Dandan Li, Yuxiong Feng, Jideofor Ezike, Russell R Elmes, M Inmaculada Barrasa and 4 more

Abstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–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

40 citing papers in PubMed.

  1. Review
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  9. Review
  10. Review
  11. Immunoregulation role of the erythroid cells.Frontiers in immunology · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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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

14 authors.

Xiaofei GaoWhitehead Institute for Biomedical Research, Cambridge, MA.ORCID 0000-0003-2799-7421
Hsiang-Ying LeeWhitehead Institute for Biomedical Research, Cambridge, MA.ORCID 0000-0002-1503-5818
Edroaldo Lummertz da RochaDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN.
Cheng ZhangDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN.
Yi-Fen LuDivision of Hematology/Oncology, Boston Children's Hospital, Boston, MA.
Dandan LiUniversity of Kansas Medical Center, Kansas City, KS.
Yuxiong FengWhitehead Institute for Biomedical Research, Cambridge, MA.
Jideofor EzikeWhitehead Institute for Biomedical Research, Cambridge, MA.
Russell R ElmesWhitehead Institute for Biomedical Research, Cambridge, MA.
M Inmaculada BarrasaWhitehead Institute for Biomedical Research, Cambridge, MA.
Patrick CahanInstitute for Cell Engineering and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD; and.
Hu LiDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN.
George Q DaleyDivision of Hematology/Oncology, Boston Children's Hospital, Boston, MA.
Harvey F LodishWhitehead Institute for Biomedical Research, Cambridge, MA.

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Michael Birnbaum · 1985 to 2026
$93.9M
TRANSCRIPTION FACTOR GATA-1 IN TERMINAL ERYTHROID DEVELOPMENTP01HL032262 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI BAUER, DANIEL EVAN · 1985 to 2021
$38.9M
NCI NIH HHS P30 CA014051NHLBI NIH HHS P01 HL032262
6 · The paper itself

Abstract

Burst-forming unit erythroid progenitors (BFU-Es) are so named based on their ability to generate in methylcellulose culture large colonies of erythroid cells that consist of "bursts" of smaller erythroid colonies derived from the later colony-forming unit erythroid progenitor erythropoietin (Epo)-dependent progenitors. "Early" BFU-E cells forming large BFU-E colonies presumably have higher capacities for self-renewal than do "late" BFU-Es forming small colonies, but the mechanism underlying this heterogeneity remains unknown. We show that the type III transforming growth factor β (TGF-β) receptor (TβRIII) is a marker that distinguishes early and late BFU-Es. Transient elevation of TβRIII expression promotes TGF-β signaling during the early BFU-E to late BFU-E transition. Blocking TGF-β signaling using a receptor kinase inhibitor increases early BFU-E cell self-renewal and total erythroblast production, suggesting the usefulness of this type of drug in treating Epo-unresponsive anemias.

Indexed as

AnemiaAnimalsAntigens, DifferentiationErythrocytesErythroid Precursor CellsErythropoietinHumansMiceProteoglycansReceptors, Transforming Growth Factor betaSignal TransductionTransforming Growth Factor betaAntigens, DifferentiationbetaglycanErythropoietinProteoglycansReceptors, Transforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID27777239
PMCPMC5146747

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.