Evidence map›Paper›PMID 28117277›Full record

ArticleEBioMedicine2017

Loss of MyoD Promotes Fate Transdifferentiation of Myoblasts Into Brown Adipocytes.

Chao Wang, Weiyi Liu, Yaohui Nie, Mulan Qaher, Hannah Elizabeth Horton, Feng Yue, Atsushi Asakura, Shihuan Kuang

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 75 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

8 authors at 2 institutions in 1 country.

Chao WangDepartment of Animal Science, Purdue University, West Lafayette, IN, USA.
Weiyi LiuDepartment of Animal Science, Purdue University, West Lafayette, IN, USA.
Yaohui NieDepartment of Animal Science, Purdue University, West Lafayette, IN, USA.
Mulan QaherStem Cell Institute, Paul and Sheila Wellstone Muscular Dystrophy Center, and Department of Neurology, University of Minnesota Medical School, Minneapolis, MN, USA.
Hannah Elizabeth HortonDepartment of Biological Sciences, Purdue University, West Lafayette, IN, USA.
Feng YueDepartment of Animal Science, Purdue University, West Lafayette, IN, USA.
Atsushi AsakuraStem Cell Institute, Paul and Sheila Wellstone Muscular Dystrophy Center, and Department of Neurology, University of Minnesota Medical School, Minneapolis, MN, USA.
Shihuan KuangDepartment of Animal Science, Purdue University, West Lafayette, IN, USA; Center for Cancer Research, Purdue University, West Lafayette, IN, USA. Electronic address: skuang@purdue.edu.
Purdue University West Lafayette · USUniversity of Minnesota · US

Funding

Notch Regulation of Stem Cell Fate in MuscleR01AR060652 · NIAMS · PURDUE UNIVERSITY · PI KUANG, SHIHUAN · 2010 to 2014
$1.6M
Genetically Engineered Muscle Stem Cell Transplantation for Muscular Dystrophy...R01AR062142 · NIAMS · UNIVERSITY OF MINNESOTA · PI ASAKURA, ATSUSHI · 2012 to 2016
$1.6M
Engineering iPSC-Derived Skeletal Muscle and Cells for TransplantationR21AR070319 · NIAMS · UNIVERSITY OF MINNESOTA · PI ASAKURA, ATSUSHI · 2016 to 2017
$372k
6 · The paper itself

Abstract

Brown adipose tissue (BAT) represents a promising agent to ameliorate obesity and other metabolic disorders. However, the abundance of BAT decreases with age and BAT paucity is a common feature of obese subjects. As brown adipocytes and myoblasts share a common Myf5 lineage origin, elucidating the molecular mechanisms underlying the fate choices of brown adipocytes versus myoblasts may lead to novel approaches to expand BAT mass. Here we identify MyoD as a key negative regulator of brown adipocyte development. CRISPR/CAS9-mediated deletion of MyoD in C2C12 myoblasts facilitates their adipogenic transdifferentiation. MyoD knockout downregulates miR-133 and upregulates the miR-133 target Igf1r, leading to amplification of PI3K-Akt signaling. Accordingly, inhibition of PI3K or Akt abolishes the adipogenic gene expression of MyoD null myoblasts. Strikingly, loss of MyoD converts satellite cell-derived primary myoblasts to brown adipocytes through upregulation of Prdm16, a target of miR-133 and key determinant of brown adipocyte fate. Conversely, forced expression of MyoD in brown preadipocytes blocks brown adipogenesis and upregulates the expression of myogenic genes. Importantly, miR-133a knockout significantly blunts the inhibitory effect of MyoD on brown adipogenesis. Our results establish MyoD as a negative regulator of brown adipocyte development by upregulating miR-133 to suppress Akt signaling and Prdm16.

Indexed as

Adipocytes, BrownAdipogenesisAnimalsBase SequenceBlotting, WesternCell LineCells, CulturedCell TransdifferentiationCRISPR-Cas SystemsDNA-Binding ProteinsGene Expression RegulationMaleMice, KnockoutMicroRNAsMicroscopy, FluorescenceMyoblastsDNA-Binding ProteinsMicroRNAsMirn133 microRNA, mouseMyoD1 myogenic differentiation proteinMyoD ProteinPrdm16 protein, mouseProto-Oncogene Proteins c-aktReceptor, IGF Type 1Transcription FactorsAdipogenesisBrown adipocytesCRISPR-Cas9MyoDMyogenesisRepressor

Identifiers

PMID28117277
PMCPMC5474440
OpenAlexW2578050788

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.