Evidence map›Paper›PMID 29641990›Full record

ArticleStem cell reports2018

HDAC1 and HDAC2 Modulate TGF-β Signaling during Endothelial-to-Hematopoietic Transition.

Roshana Thambyrajah, Muhammad Z H Fadlullah, Martin Proffitt, Rahima Patel, Shaun M Cowley, Valerie Kouskoff, Georges Lacaud

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2018. 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
1.8field-weighted citation impact, top 17% 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, 41 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Roshana ThambyrajahCRUK Stem Cell Biology Group, CRUK Manchester Institute, 555 Wilmslow Road, Manchester M20 4GJ, UK.
Muhammad Z H FadlullahCRUK Stem Cell Biology Group, CRUK Manchester Institute, 555 Wilmslow Road, Manchester M20 4GJ, UK.
Martin ProffittCRUK Stem Cell Biology Group, CRUK Manchester Institute, 555 Wilmslow Road, Manchester M20 4GJ, UK.
Rahima PatelCRUK Stem Cell Biology Group, CRUK Manchester Institute, 555 Wilmslow Road, Manchester M20 4GJ, UK.
Shaun M CowleyDepartment of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester LE1 7RH, UK.
Valerie KouskoffDivision of Developmental Biology & Medicine, The University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK. Electronic address: valerie.kouskoff@manchester.ac.uk.
Georges LacaudCRUK Stem Cell Biology Group, CRUK Manchester Institute, 555 Wilmslow Road, Manchester M20 4GJ, UK. Electronic address: georges.lacaud@manchester.ac.uk.
Cancer Research UK Manchester Institute · GBUniversity of Leicester · GBUniversity of Manchester · GB

Funding

Biotechnology and Biological Sciences Research Council BB/I001794/1Cancer Research UK 12486Cancer Research UK 12487Cancer Research UK 19565Medical Research Council MR/J009202/1Medical Research Council MR/P000673/1
6 · The paper itself

Abstract

The first hematopoietic stem and progenitor cells are generated during development from hemogenic endothelium (HE) through trans-differentiation. The molecular mechanisms underlying this endothelial-to-hematopoietic transition (EHT) remain poorly understood. Here, we explored the role of the epigenetic regulators HDAC1 and HDAC2 in the emergence of these first blood cells in vitro and in vivo. Loss of either of these epigenetic silencers through conditional genetic deletion reduced hematopoietic transition from HE, while combined deletion was incompatible with blood generation. We investigated the molecular basis of HDAC1 and HDAC2 requirement and identified TGF-β signaling as one of the pathways controlled by HDAC1 and HDAC2. Accordingly, we experimentally demonstrated that activation of this pathway in HE cells reinforces hematopoietic development. Altogether, our results establish that HDAC1 and HDAC2 modulate TGF-β signaling and suggest that stimulation of this pathway in HE cells would be beneficial for production of hematopoietic cells for regenerative therapies.

Indexed as

HematopoiesisSignal TransductionAnimalsBenzamidesCell DifferentiationDioxolesEndothelial CellsGene DeletionHemangioblastsHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase InhibitorsMiceTransforming Growth Factor beta4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamideBenzamidesDioxolesHdac1 protein, mouseHdac2 protein, mouseHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase InhibitorsTransforming Growth Factor betaAGMembryonic stem cellsendothelial-to-hematopoietic transitionepigeneticHDAC1HDAC2hematopoietic stem cellshemogenic endotheliumin vitro differentiationTGF-β signaling

Identifiers

PMID29641990
PMCPMC5998800
OpenAlexW2792755870

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.