Evidence map›Paper›PMID 35035705›Full record

ArticleAmerican journal of translational research2021

MiR-200c-3p affects cochlear hair cells damaged by oxidative stress via modulating Taok1 expression.

Lihua Wu, Ning Yang, Qinghua Liu, Yue Bai, Bo Gao

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 58% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Correction to "MiR-200c-3p as a Novel Genetic Marker and Therapeutic Tool for Alopecia Areata".Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2025
    Article
  2. Article
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

5 authors at 3 institutions in 1 country.

Lihua WuDepartment of Otolaryngology, Head and Neck Surgery, Fujian Medical University ShengLi Clinical College, Fujian Provincial Hospital Fuzhou 350001, Fujian, China.
Ning YangDepartment of Otolaryngology, Head and Neck Surgery, First Affiliated Hospital of China Medical University Shenyang 110001, Liaoning, China.
Qinghua LiuDepartment of Otolaryngology, Head and Neck Surgery, Fujian Medical University ShengLi Clinical College, Fujian Provincial Hospital Fuzhou 350001, Fujian, China.
Yue BaiDepartment of Ophthalmology, The First Affiliated Hospital of Fujian Medical University Fuzhou 350005, Fujian, China.
Bo GaoDepartment of Otolaryngology, Head and Neck Surgery, Institute of Otolaryngology, Chinese PLA General Hospital Beijing 100036, China.
Fujian Medical University · CNChinese PLA General Hospital · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe aim of this study was to elucidate the role of miR-200c-3p in cochlear hair cells injured by oxidative stress (OS) and the underlying mechanisms.

methodsThe OS injury model of HEI-OC1 cells was induced by 100 μmol/L tert-butyl hydroperoxide (t-BHP). The expression of miR-200c-3p in HEI-OC1 was detected by RT-PCR, the levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), Catalase (CAT), and malondialdehyde (MDA) were determined with ELISA, and the expression levels of Taok1 and apoptosis-related proteins were measured by Western Blot. Flow cytometry was used to detect cell apoptosis.

resultsReal-time polymerase chain reaction (RT-qPCR) analysis identified down-regulated miR-200c-3p and up-regulated Taok1 in HEI-OC1 cells damaged by OS, as well as an inverse association between miR-200c-3p and Taok1. Cell tests confirmed that miR-200c-3p overexpression could effectively inhibit the OS response and apoptosis of HEI-OC1 cells. Bioinformatics prediction and dual luciferase reporter assay revealed that Taok1 was a direct target of miR-200c-3p. Taok1 overexpression could reverse the protective action of miR-200c-3p overexpression on the OS injury of HEI-OC1 cells.

conclusionsGiven the capacity of miR-200c-3p to suppress the OS and apoptosis of HEI-OC1 cells via targeting Taok1, it can be a novel and potential therapeutic target for cochlear hair cell injury.

Indexed as

apoptosiscochlear hair cellsmiR-200c-3poxidative stresstaok1

Identifiers

PMID35035705
PMCPMC8748156
OpenAlexW4206871976

What OpenQuestion holds

Textmetadata
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.