Evidence map›Paper›PMID 28669599›Full record

ArticleStem cell reports2017

Inactivation of STAT3 Signaling Impairs Hair Cell Differentiation in the Developing Mouse Cochlea.

Qianqian Chen, Yizhou Quan, Naitao Wang, Chengying Xie, Zhongzhong Ji, Hao He, Renjie Chai, Huawei Li, Shankai Yin, Y Eugene Chin and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell reports, 2017. 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
0.8field-weighted citation impact, top 33% 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, 21 citations in OpenAlex.

  1. Review
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  12. IL22 Inhibits Epithelial Stem Cell Expansion in an Ileal Organoid Model.Cellular and molecular gastroenterology and hepatology · 2019
    Article
  13. STAT3, stem cells, cancer stem cells and p63.Cellular & molecular biology letters · 2018
    Review
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

12 authors at 6 institutions in 1 country.

Qianqian ChenState Key Laboratory of Oncogenes and Related Genes, Renji-MedX Stem Cell Research Center, Ren Ji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Med-X Research Institute & School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Yizhou QuanState Key Laboratory of Oncogenes and Related Genes, Renji-MedX Stem Cell Research Center, Ren Ji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Med-X Research Institute & School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Naitao WangState Key Laboratory of Oncogenes and Related Genes, Renji-MedX Stem Cell Research Center, Ren Ji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Chengying XieMed-X Research Institute & School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Zhongzhong JiState Key Laboratory of Oncogenes and Related Genes, Renji-MedX Stem Cell Research Center, Ren Ji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Med-X Research Institute & School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Hao HeMed-X Research Institute & School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; The Affiliated Six People's Hospital, Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Renjie ChaiMOE Key Laboratory of Developmental Genes and Human Disease, Institute of Life Sciences, Southeast University, Nanjing 210096, China.
Huawei LiOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, China.
Shankai YinThe Affiliated Six People's Hospital, Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Y Eugene ChinChina Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences-Shanghai Jiao Tong University School of Medicine, Shanghai 200031, China.
Xunbin WeiState Key Laboratory of Oncogenes and Related Genes, Renji-MedX Stem Cell Research Center, Ren Ji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Med-X Research Institute & School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China. Electronic address: xwei01@sjtu.edu.cn.
Wei-Qiang GaoState Key Laboratory of Oncogenes and Related Genes, Renji-MedX Stem Cell Research Center, Ren Ji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Med-X Research Institute & School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; The Affiliated Six People's Hospital, Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China. Electronic address: gao.weiqiang@sjtu.edu.cn.
Shanghai Jiao Tong University · CNState Key Laboratory of Oncogene and Related Genes · CNShanghai Sixth People's Hospital · CNChinese Academy of Sciences · CNSoutheast University · CNState Key Laboratory of Medical Neurobiology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although STAT3 signaling is demonstrated to regulate sensory cell differentiation and regeneration in the zebrafish, its exact role is still unclear in mammalian cochleae. Here, we report that STAT3 and its activated form are specifically expressed in hair cells during mouse cochlear development. Importantly, conditional cochlear deletion of Stat3 leads to an inhibition on hair cell differentiation in mice in vivo and in vitro. By cell fate analysis, inactivation of STAT3 signaling shifts the cell division modes from asymmetric to symmetric divisions from supporting cells. Moreover, inhibition of Notch signaling stimulates STAT3 phosphorylation, and inactivation of STAT3 signaling attenuates production of supernumerary hair cells induced by a Notch pathway inhibitor. Our findings highlight an important role of the STAT3 signaling during mouse cochlear hair cell differentiation and may have clinical implications for the recovery of hair cell loss-induced hearing impairment.

Indexed as

Cell DifferentiationSignal TransductionAnimalsCell DivisionCells, CulturedCochleaGene DeletionGene Expression Regulation, DevelopmentalHair Cells, AuditoryMiceReceptors, NotchSTAT3 Transcription FactorReceptors, NotchStat3 protein, mouseSTAT3 Transcription Factorcell division modecell fate specificationhair cellNotch signalingSTAT3 signalingsupporting cell

Identifiers

PMID28669599
PMCPMC5511372
OpenAlexW2731873738

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.