Evidence map›Paper›PMID 22535663›Full record

ArticleBlood2012

A critical role for endoglin in the emergence of blood during embryonic development.

Luciene Borges, Michelina Iacovino, Timothy Mayerhofer, Naoko Koyano-Nakagawa, June Baik, Daniel J Garry, Michael Kyba, Michelle Letarte, Rita C R Perlingeiro

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 2 institutions in 2 countries.

Luciene BorgesDepartment of Medicine, Lillehei Heart Institute, University of Minnesota, Minneapolis, MN 55455, USA.
Michelina Iacovino
Timothy Mayerhofer
Naoko Koyano-Nakagawa
June Baik
Daniel J Garry
Michael Kyba
Michelle Letarte
Rita C R Perlingeiro
Minneapolis Heart Institute Foundation · USHospital for Sick Children · CA

Funding

Midwestern Progenitor Cell ConsortiumU01HL100407 · NHLBI · UNIVERSITY OF MINNESOTA · PI GARRY, DANIEL J., KYBA, MICHAEL · 2009 to 2015
$7.8M
The Role of Endoglin in Hemangioblast DevelopmentR01HL085840 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI PERLINGEIRO, RITA C. R. · 2007 to 2011
$1.9M
Transcriptional Regulation of Cardiac MorphogenesisR01HL085729 · NHLBI · UNIVERSITY OF MINNESOTA · PI GARRY, DANIEL J. · 2009 to 2010
$972k
NHLBI NIH HHS R01 HL085729NHLBI NIH HHS R01 HL085840NHLBI NIH HHS R01 HL085840-01NHLBI NIH HHS U01 HL100407
6 · The paper itself

Abstract

Much remains unknown about the signals that induce early mesoderm to initiate hematopoietic differentiation. Here, we show that endoglin (Eng), a receptor for the TGFβ superfamily, identifies all cells with hematopoietic fate in the early embryo. These arise in an Eng(+)Flk1(+) mesodermal precursor population at embryonic day 7.5 (E7.5), a cell fraction also endowed with endothelial potential. In Eng-knockout embryos, hematopoietic colony activity and numbers of CD71(+)Ter119(+) erythroid progenitors were severely reduced. This coincided with severely reduced expression of embryonic globin and key bone morphogenic protein (BMP) target genes, including the hematopoietic regulators Scl, Gata1, Gata2, and Msx-1. To interrogate molecular pathways active in the earliest hematopoietic progenitors, we applied transcriptional profiling to sorted cells from E7.5 embryos. Eng(+)Flk-1(+) progenitors coexpressed TGFβ and BMP receptors and target genes. Furthermore, Eng(+)Flk-1(+) cells presented high levels of phospho-SMAD1/5, indicating active TGFβ and/or BMP signaling. Remarkably, under hematopoietic serum-free culture conditions, hematopoietic outgrowth of Eng-expressing cells was dependent on the TGFβ superfamily ligands BMP4, BMP2, or TGF-β1. These data demonstrate that the E(+)F(+) fraction at E7.5 represents mesodermal cells competent to respond to TGFβ1, BMP4, or BMP2, shaping their hematopoietic development, and that Eng acts as a critical regulator in this process by modulating TGF/BMP signaling.

Indexed as

HematopoiesisAnimalsBone Morphogenetic Protein 2Bone Morphogenetic Protein 4Embryo, MammalianEmbryonic DevelopmentEndoglinGene Expression Regulation, DevelopmentalGene Knockout TechniquesHematopoietic Stem CellsIntracellular Signaling Peptides and ProteinsMiceSignal TransductionTransforming Growth Factor betaTransforming Growth Factor beta1Vascular Endothelial Growth Factor Receptor-2Bmp2 protein, mouseBmp4 protein, mouseBone Morphogenetic Protein 2Bone Morphogenetic Protein 4EndoglinEng protein, mouseIntracellular Signaling Peptides and ProteinsTransforming Growth Factor betaTransforming Growth Factor beta1Vascular Endothelial Growth Factor Receptor-2

Identifiers

PMID22535663
PMCPMC3369678
OpenAlexW2088473598

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.