Evidence map›Paper›PMID 28498863›Full record

ArticlePloS one2017

Notch ligands regulate the muscle stem-like state ex vivo but are not sufficient for retaining regenerative capacity.

Hiroshi Sakai, Sumiaki Fukuda, Miki Nakamura, Akiyoshi Uezumi, Yu-Taro Noguchi, Takahiko Sato, Mitsuhiro Morita, Harumoto Yamada, Kunihiro Tsuchida, Shahragim Tajbakhsh and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 44 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

11 authors at 4 institutions in 2 countries.

Hiroshi SakaiStem Cells & Development, Department of Developmental & Stem Cell Biology, CNRS UMR 3738, Institut Pasteur, Paris, France.
Sumiaki FukudaLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Miki NakamuraLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Akiyoshi UezumiDivision for Therapies Against Intractable Diseases, Institute for Comprehensive Medical Science, Fujita Health University, Aichi, Japan.
Yu-Taro NoguchiLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Takahiko SatoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Mitsuhiro MoritaDepartment of Orthopaedic Surgery, Fujita Health University, Aichi, Japan.
Harumoto YamadaDepartment of Orthopaedic Surgery, Fujita Health University, Aichi, Japan.
Kunihiro TsuchidaDivision for Therapies Against Intractable Diseases, Institute for Comprehensive Medical Science, Fujita Health University, Aichi, Japan.
Shahragim TajbakhshStem Cells & Development, Department of Developmental & Stem Cell Biology, CNRS UMR 3738, Institut Pasteur, Paris, France.
So-Ichiro FukadaLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.ORCID http://orcid.org/0000-0003-4051-5108
Fujita Health University · JPThe University of Osaka · JPCentre National de la Recherche Scientifique · FRKyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myogenic stem cells are a promising avenue for the treatment of muscular disorders. Freshly isolated muscle stem cells have a remarkable engraftment ability in vivo, but their cell number is limited. Current conventional culture conditions do not allow muscle stem cells to expand in vitro with their bona fide engraftment efficiency, requiring the improvement of culture procedures for achieving successful cell-therapy for muscle disorders. Here we expanded mouse muscle stem cells and human myoblasts with Notch ligands, DLL1, DLL4, and JAG1 to activate Notch signaling in vitro and to investigate whether these cells could retain their engraftment efficiency. Notch signaling promotes the expansion of Pax7+MyoD- mouse muscle stem-like cells and inhibits differentiation even after passage in vitro. Treatment with Notch ligands induced the Notch target genes and generated PAX7+MYOD- stem-like cells from human myoblasts previously cultured on conventional culture plates. However, cells treated with Notch ligands exhibit a stem cell-like state in culture, yet their regenerative ability was less than that of freshly isolated cells in vivo and was comparable to that of the control. These unexpected findings suggest that artificial maintenance of Notch signaling alone is insufficient for improving regenerative capacity of mouse and human donor-muscle cells and suggest that combinatorial events are critical to achieve muscle stem cell and myoblast engraftment potential.

Indexed as

AnimalsCalcium-Binding ProteinsCell DifferentiationCells, CulturedImmunohistochemistryIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsJagged-1 ProteinMembrane ProteinsMiceMuscle CellsMuscle DevelopmentMyoblastsMyoD ProteinPAX7 Transcription FactorReal-Time Polymerase Chain ReactionCalcium-Binding Proteinsdelta proteinDlk1 protein, mouseIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsJag1 protein, mouseJagged-1 ProteinMembrane ProteinsMyoD1 myogenic differentiation proteinMyoD ProteinPax7 protein, mousePAX7 Transcription FactorReceptors, Notch

Identifiers

PMID28498863
PMCPMC5428926
OpenAlexW2612350007

What OpenQuestion holds

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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.