Evidence map›Paper›PMID 30925184›Full record

ArticlePloS one2019

Loss of miR-451a enhances SPARC production during myogenesis.

Rachel Munk, Jennifer L Martindale, Xiaoling Yang, Jen-Hao Yang, Ioannis Grammatikakis, Clara Di Germanio, Sarah J Mitchell, Rafael de Cabo, Elin Lehrmann, Yongqing Zhang and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

8 citing papers in PubMed, 12 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

15 authors at 2 institutions in 2 countries.

Rachel MunkLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Jennifer L MartindaleLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Xiaoling YangLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Jen-Hao YangLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Ioannis GrammatikakisLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Clara Di GermanioTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Sarah J MitchellTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Rafael de CaboTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Elin LehrmannLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Yongqing ZhangLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Kevin G BeckerLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Vered RazDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Myriam GorospeLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.ORCID 0000-0001-5439-3434
Kotb AbdelmohsenLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Amaresh C PandaLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
National Institutes of Health · USLeiden University Medical Center · NL

Funding

Post-transcriptional regulation of energy usage: glucose and lipid metabolismZIAAG000394 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$18.7M
Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
Aging Intervention ProgramZIAAG000363 · NIA · NATIONAL INSTITUTE ON AGING · PI DE CABO, RAFAEL · 2009 to 2025
$9.0M
Post-transcriptional Regulation Of Proliferative and Stress Response GenesZ01AG000511 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM NONE · 1998 to 2008
$1.6M
Intramural NIH HHS Z01 AG000511
6 · The paper itself

Abstract

MicroRNAs (miRNAs) are small noncoding RNAs that critically regulate gene expression. Their abundance and function have been linked to a range of physiologic and pathologic processes. In aged monkey muscle, miR-451a and miR-144-3p were far more abundant than in young monkey muscle. This observation led us to hypothesize that miR-451a and miR-144-3p may influence muscle homeostasis. To test if these conserved microRNAs were implicated in myogenesis, we investigated their function in the mouse myoblast line C2C12. The levels of both microRNAs declined with myogenesis; however, only overexpression of miR-451a, but not miR-144-3p, robustly impeded C2C12 differentiation, suggesting an inhibitory role for miR-451a in myogenesis. Further investigation of the regulatory influence of miR-451a identified as one of the major targets Sparc mRNA, which encodes a secreted protein acidic and rich in cysteine (SPARC) that functions in wound healing and cellular differentiation. In mouse myoblasts, miR-451a suppressed Sparc mRNA translation. Together, our findings indicate that miR-451a is downregulated in differentiated myoblasts and suggest that it decreases C2C12 differentiation at least in part by suppressing SPARC biosynthesis.

Indexed as

Muscle Development3' Untranslated RegionsAnimalsCell LineCell ProliferationMiceMicroRNAsMyoblastsOsteonectinPolyribosomesProtein Biosynthesis3' Untranslated RegionsMicroRNAsMirn451 microRNA, mouseOsteonectinSPARC protein, mouse

Identifiers

PMID30925184
PMCPMC6440632
OpenAlexW2927464575

What OpenQuestion holds

Textmetadata
LicenceCC0
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.