Evidence map›Paper›PMID 35043940›Full record

ArticleDevelopment (Cambridge, England)2022

MyD88-dependent TLR signaling oppositely regulates hematopoietic progenitor and stem cell formation in the embryo.

Laura F Bennett, Melanie D Mumau, Yan Li, Nancy A Speck

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Gpr171 regulates embryonic hematopoietic stem cell emergence via ERK1/2 and Notch signaling.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

4 authors at 2 institutions in 2 countries.

Laura F BennettAbramson Family Cancer Research Institute and Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.ORCID 0000-0002-4046-0736
Melanie D MumauAbramson Family Cancer Research Institute and Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Yan LiDepartment of Veterinary Medicine and Institute of Preventive Veterinary Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, People's Republic of China.
Nancy A SpeckAbramson Family Cancer Research Institute and Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.ORCID 0000-0002-1893-582X
Cancer Research Institute · USZhejiang University · CN

Funding

HEMATOLOGY CLINICAL RESEARCH TRAINING PROGRAMT32HL007439 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LAWRENCE F BRASS, PETER S KLEIN · 1985 to 2026
$17.1M
Biochemistry of Leukemia Virus Core-Binding FactorR01HL091724 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI SPECK, NANCY · 2008 to 2024
$8.3M
HEMATOPOIESIS TRAINING GRANTT32DK007780 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI TONG, WEI · 1999 to 2023
$6.7M
NHLBI NIH HHS R01 HL091724NHLBI NIH HHS T32 HL007439NIDDK NIH HHS T32 DK007780
6 · The paper itself

Abstract

Hemogenic endothelial (HE) cells in the dorsal aorta undergo an endothelial-to-hematopoietic transition (EHT) to form multipotent progenitors, lympho-myeloid biased progenitors (LMPs), pre-hematopoietic stem cells (pre-HSCs) and adult-repopulating HSCs. These briefly accumulate in intra-arterial hematopoietic clusters (IAHCs) before being released into the circulation. It is generally assumed that the number of IAHC cells correlates with the number of HSCs. Here, we show that changes in the number of IAHC cells, LMPs and HSCs can be uncoupled. Mutations impairing MyD88-dependent toll-like receptor (TLR) signaling decreased the number of IAHC cells and LMPs, but increased the number of HSCs in the aorta-gonad-mesonephros region of mouse embryos. TLR4-deficient embryos generated normal numbers of HE cells, but IAHC cell proliferation decreased. Loss of MyD88-dependent TLR signaling in innate immune myeloid cells had no effect on IAHC cell numbers. Instead, TLR4 deletion in endothelial cells (ECs) recapitulated the phenotype observed with germline deletion, demonstrating that MyD88-dependent TLR signaling in ECs and/or in IAHCs regulates the numbers of LMPs and HSCs.

Indexed as

Signal TransductionAnimalsCell DifferentiationCore Binding Factor Alpha 2 SubunitEmbryo, MammalianEndothelial CellsHemangioblastsHematopoietic Stem CellsImmunity, InnateMiceMice, Inbred C57BLMice, KnockoutMyeloid CellsMyeloid Differentiation Factor 88Toll-Like Receptor 4Toll-Like ReceptorsCore Binding Factor Alpha 2 SubunitMyeloid Differentiation Factor 88Runx1 protein, mouseTlr4 protein, mouseToll-Like Receptor 4Toll-Like ReceptorsAGM regionHematopoietic stem cellsHemogenic endothelial cellsInflammationToll-like receptor

Identifiers

PMID35043940
PMCPMC8935211
OpenAlexW4226271800

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.