Evidence map›Paper›PMID 27758863›Full record

ArticleThe Journal of biological chemistry2016

Mesenchymal Stromal Cell-derived Extracellular Vesicles Promote Myeloid-biased Multipotent Hematopoietic Progenitor Expansion via Toll-Like Receptor Engagement.

Natalya A Goloviznina, Santhosh Chakkaramakkil Verghese, Young Me Yoon, Oleh Taratula, Daniel L Marks, Peter Kurre

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Natalya A GolovizninaFrom the Department of Pediatrics.
Santhosh Chakkaramakkil VergheseFrom the Department of Pediatrics,; Papé Family Pediatric Research Institute, and.
Young Me YoonFrom the Department of Pediatrics,; Papé Family Pediatric Research Institute, and.
Oleh Taratulathe Oregon State University, College of Pharmacy, Corvallis, Oregon 97331.
Daniel L MarksFrom the Department of Pediatrics,; Papé Family Pediatric Research Institute, and.
Peter KurreFrom the Department of Pediatrics,; Papé Family Pediatric Research Institute, and; Pediatric Cancer Biology Program, Oregon Health & Science University, Portland, Oregon 97239 and. Electronic address: kurrepe@ohsu.edu.
Pediatrics and Genetics · USFamily Research Institute · USOregon State University · USPulp and Paper Research Institute · SK

Funding

Upgrade of confocal microscopy at the Oregon National Primate Research CenterP51OD011092 · OD · OREGON HEALTH & SCIENCE UNIVERSITY · PI Bonnie J. Nagel · 2012 to 2026
$203.9M
PREPARATION AND DISTRUBUTION OF ADULT STEM CELLS: HUMAN &RODENTP40RR017447 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI PROCKOP, DARWIN JOHNSON · 2003 to 2011
$8.9M
(PQD6) Hypothalamic Inflammation in the Initiation of CachexiaR01CA184324 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI MARKS, DANIEL L. · 2014 to 2017
$1.8M
Stem Cell Biology Training ProgramT32GM113846 · NIGMS · UNIVERSITY OF MINNESOTA · PI PERLINGEIRO, RITA C. R. · 2015 to 2019
$712k
NCI NIH HHS R01 CA184324NCRR NIH HHS P40 RR017447NIGMS NIH HHS T32 GM113846NIH HHS P51 OD011092
6 · The paper itself

Abstract

Mesenchymal stromal cells (MSCs) present in the bone marrow microenvironment secrete cytokines and angiogenic factors that support the maintenance and regenerative expansion of hematopoietic stem and progenitor cells (HSPCs). Here, we tested the hypothesis that extracellular vesicles (EVs) released by MSCs contribute to the paracrine crosstalk that shapes hematopoietic function. We systematically characterized EV release by murine stromal cells and demonstrate that MSC-derived EVs prompt a loss of HSPC quiescence with concomitant expansion of murine myeloid progenitors. Our studies reveal that HSPC expansion by MSC EVs is mediated via the MyD88 adapter protein and is partially blocked by treatment with a TLR4 inhibitor. Imaging of fluorescence protein-tagged MSC EVs corroborated their cellular co-localization with TLR4 and endosomal Rab5 compartments in HSPCs. The dissection of downstream responses to TLR4 activation reveals that the mechanism by which MSC EVs impact HSPCs involves canonical NF-κB signaling and downstream activation of Hif-1α and CCL2 target genes. Our aggregate data identify a previously unknown role for MSC-derived EVs in the regulation of hematopoiesis through innate immune mechanisms and illustrate the expansive cell-cell crosstalk in the bone marrow microenvironment.

Indexed as

AnimalsCell-Derived MicroparticlesChemokine CCL2Hematopoietic Stem CellsHypoxia-Inducible Factor 1, alpha SubunitMesenchymal Stem CellsMiceMyeloid Differentiation Factor 88rab5 GTP-Binding ProteinsToll-Like Receptor 4Ccl2 protein, mouseChemokine CCL2Hif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitMyd88 protein, mouseMyeloid Differentiation Factor 88rab5 GTP-Binding ProteinsTlr4 protein, mouseToll-Like Receptor 4exosome (vesicle)extracellular vesicleshematopoiesishematopoietic stem cellsmesenchymal stem cells (MSCs)microenvironmentToll-like receptor (TLR)

Identifiers

PMID27758863
PMCPMC5114412
OpenAlexW2528229495

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.