Evidence map›Paper›PMID 27121005›Full record

ArticleBMC genomics2016

MiR-210 promotes sensory hair cell formation in the organ of corti.

Sabrina Riccardi, Sebastian Bergling, Frederic Sigoillot, Martin Beibel, Annick Werner, Juliet Leighton-Davies, Judith Knehr, Tewis Bouwmeester, Christian N Parker, Guglielmo Roma and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  3. NcRNA: key and potential in hearing loss.Frontiers in neuroscience · 2023
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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 3 institutions in 2 countries.

Sabrina RiccardiDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Sebastian BerglingDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Frederic SigoillotDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Cambridge, USA.
Martin BeibelDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Annick WernerDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Juliet Leighton-DaviesDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Judith KnehrDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Tewis BouwmeesterDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Christian N ParkerDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Guglielmo RomaDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland.
Bernd KinzelDevelopmental and Molecular Pathways, Novartis Institute for Biomedical Research, Basel, Switzerland. bernd.kinzel@novartis.com.
Novartis Institutes for BioMedical ResearchNovartis (Switzerland) · CHPathways Behavioral Services · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHearing loss is the most common sensory defect afflicting several hundred million people worldwide. In most cases, regardless of the original cause, hearing loss is related to the degeneration and death of hair cells and their associated spiral ganglion neurons. Despite this knowledge, relatively few studies have reported regeneration of the auditory system. Significant gaps remain in our understanding of the molecular mechanisms underpinning auditory function, including the factors required for sensory cell regeneration. Recently, the identification of transcriptional activators and repressors of hair cell fate has been augmented by the discovery of microRNAs (miRNAs) associated with hearing loss. As miRNAs are central players of differentiation and cell fate, identification of miRNAs and their gene targets may reveal new pathways for hair cell regeneration, thereby providing new avenues for the treatment of hearing loss.

resultsIn order to identify new genetic elements enabling regeneration of inner ear sensory hair cells, next-generation miRNA sequencing (miRSeq) was used to identify the most prominent miRNAs expressed in the mouse embryonic inner ear cell line UB/OC-1 during differentiation towards a hair cell like phenotype. Based on these miRSeq results eight most differentially expressed miRNAs were selected for further characterization. In UB/OC-1, miR-210 silencing in vitro resulted in hair cell marker expression, whereas ectopic expression of miR-210 resulted in new hair cell formation in cochlear explants. Using a lineage tracing mouse model, transdifferentiation of supporting epithelial cells was identified as the likely mechanism for this new hair cell formation. Potential miR-210 targets were predicted in silico and validated experimentally using a miR-trap approach.

conclusionMiRSeq followed by ex vivo validation revealed miR-210 as a novel factor driving transdifferentiation of supporting epithelial cells to sensory hair cells suggesting that miR-210 might be a potential new factor for hearing loss therapy. In addition, identification of inner ear pathways regulated by miR-210 identified potential new drug targets for the treatment of hearing loss.

Indexed as

Cell TransdifferentiationRegenerationAnimalsCell LineGene Knock-In TechniquesHair Cells, Auditory, InnerHigh-Throughput Nucleotide SequencingMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicMicroRNAsOrgan Culture TechniquesOrgan of CortiSequence Analysis, RNASOXB1 Transcription FactorsMicroRNAsMIRN210 microRNA, mouseSox2 protein, mouseSOXB1 Transcription FactorsHearing lossMiR-210Next generation sequencingTransdifferentiation

Identifiers

PMID27121005
PMCPMC4848794
OpenAlexW2342737631

What OpenQuestion holds

Textmetadata
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.