Evidence map›Paper›PMID 31939628›Full record

ArticleMolecular medicine reports2020

Increased mitochondrial DNA copy number protects hair cells and HEI‑OC1 cells against drug‑induced apoptosis.

Honglin Mei, Dongmei Mei, Huiqian Yu, Shan Sun, Yan Chen, Yanping Zhang, Renjie Chai, Huawei Li

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

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 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

8 authors at 4 institutions in 1 country.

Honglin Mei *ENT Institute and Department of Otorhinolaryngology, Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, P.R. China.
Dongmei Mei *Department of Stomatology, Key Laboratory of Oral Clinical Medicine, The Affiliated Hospital of Qingdao University, College of Stomatology, Qingdao University, Qingdao, Shandong 266000, P.R. China.
Huiqian Yu *ENT Institute and Department of Otorhinolaryngology, Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, P.R. China.
Shan SunENT Institute and Department of Otorhinolaryngology, Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, P.R. China.
Yan ChenENT Institute and Department of Otorhinolaryngology, Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, P.R. China.
Yanping ZhangENT Institute and Department of Otorhinolaryngology, Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, P.R. China.
Renjie ChaiCo‑Innovation Center of Neuroregeneration, Key Laboratory for Developmental Genes and Human Disease, Ministry of Education, Institute of Life Sciences, Southeast University, Nanjing, Jiangsu 210096, P.R. China.
Huawei LiENT Institute and Department of Otorhinolaryngology, Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, P.R. China.
Eye & ENT Hospital of Fudan University · CNState Key Laboratory of Medical NeurobiologyQingdao University · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several factors trigger apoptosis in cochlear hair cells. Previous studies have shown that mitochondria play key roles in apoptosis, but the role of mitochondrial deoxyribonucleic acid (mtDNA) copy number in the pathogenesis of hair cell apoptosis remains largely unknown. We used mouse cochlear hair cells and House Ear Institute‑Organ of Corti 1 (HEI‑OC1) cells to explore the relationship between mtDNA copy number and cell apoptosis. We found that the mtDNA copy number of hair cells was reduced relative to mitochondrial mass and hypothesized that increasing it might have a protective effect. We then increased the mtDNA copy number of the hair and HEI‑OC1 cells by transfecting them with an adeno‑associated virus (AAV) vector containing mitochondrial transcription factor A (TFAM). We found that the apoptosis rates decreased upon inducing apoptosis with neomycin or cisplatin (DDP). To elucidate the mechanisms, we analyzed the mitochondrial‑membrane permeability and mitochondrial function of HEI‑OC1 cells. Our results suggested that the increase in mtDNA copy number could protect hair cells and HEI‑OC1 cells against drug‑induced apoptosis by stabilizing the permeability of the mitochondrial membrane and mitochondrial function.

Indexed as

AnimalsApoptosisCells, CulturedCisplatinDependovirusDNA-Binding ProteinsDNA Copy Number VariationsDNA, MitochondrialFemaleGenetic VectorsHair Cells, AuditoryIn Situ Hybridization, FluorescenceMaleMiceMice, Inbred C57BLMitochondriaCisplatinDNA-Binding ProteinsDNA, MitochondrialMitochondrial Proteinsmitochondrial transcription factor ANeomycinReactive Oxygen SpeciesTranscription Factorsapoptosiscochlear hair cellsHei-oc1mitochondrial dna copy numbermitochondrial permeability

Identifiers

PMID31939628
PMCPMC6896317
OpenAlexW2991264751

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.