Evidence map›Paper›PMID 20856896›Full record

ArticlePloS one2010

β1-syntrophin modulation by miR-222 in mdx mice.

Valeria De Arcangelis, Filippo Serra, Carlo Cogoni, Elisabetta Vivarelli, Lucia Monaco, Fabio Naro

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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  9. Non-coding RNAs in muscle dystrophies.International journal of molecular sciences · 2013
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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

6 authors at 2 institutions in 1 country.

Valeria De ArcangelisDepartment of Histology and Medical Embryology, University Sapienza, Rome, Italy.
Filippo Serra
Carlo Cogoni
Elisabetta Vivarelli
Lucia Monaco
Fabio Naro
Sapienza University of Rome · ITUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn mdx mice, the absence of dystrophin leads to the deficiency of other components of the dystrophin-glycoprotein complex (DAPC), making skeletal muscle fibers more susceptible to necrosis. The mechanisms involved in the disappearance of the DAPC are not completely understood. The muscles of mdx mice express normal amounts of mRNA for the DAPC components, thus suggesting post-transcriptional regulation. METHODOLOGY/PRINCIPAL

findingsWe investigated the hypothesis that DAPC reduction could be associated with the microRNA system. Among the possible microRNAs (miRs) found to be upregulated in the skeletal muscle tissue of mdx compared to wt mice, we demonstrated that miR-222 specifically binds to the 3'-UTR of β1-syntrophin and participates in the downregulation of β1-syntrophin. In addition, we documented an altered regulation of the 3'-UTR of β1-syntrophin in muscle tissue from dystrophic mice. CONCLUSION/SIGNIFICANCE: These results show the importance of the microRNA system in the regulation of DAPC components in dystrophic muscle, and suggest a potential role of miRs in the pathophysiology of dystrophy.

Indexed as

3' Untranslated RegionsAnimalsChlorocebus aethiopsCOS CellsDown-RegulationDystroglycansDystrophin-Associated ProteinsGene Expression RegulationGlycoproteinsMiceMice, Inbred mdxMice, TransgenicMicroRNAsMuscle, SkeletalMuscular Dystrophy, DuchenneProtein Isoforms3' Untranslated RegionsDystroglycansDystrophin-Associated ProteinsGlycoproteinsMicroRNAsMIRN222 microRNA, mouseProtein IsoformsRNA, Messengersyntrophin

Identifiers

PMID20856896
PMCPMC2938373
OpenAlexW1963536707

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.