Evidence map›Paper›PMID 25929858›Full record

ArticleCell death and differentiation2015

Live imaging the phagocytic activity of inner ear supporting cells in response to hair cell death.

E L Monzack, L A May, S Roy, J E Gale, L L Cunningham

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 56 citations in OpenAlex.

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  14. Expression of Calbindin-D28K in the Developing and Adult Mouse Cochlea.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022
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  15. Review
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  19. Engulfed by Glia: Glial Pruning in Development, Function, and Injury across Species.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
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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

5 authors at 3 institutions in 2 countries.

E L MonzackNational Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
L A MayNational Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
S RoyNational Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
J E GaleUCL Ear Institute, University College, London WC1X 8EE, UK.
L L CunninghamNational Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
National Institute on Deafness and Other Communication Disorders · USNational Institutes of Health · USUniversity College London · GB

Funding

Mechanisms of Sensory Hair Cell Survival and DeathZIADC000079 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI CUNNINGHAM, LISA L · 2011 to 2025
$27.2M
Intramural NIH HHS ZIA DC000079
6 · The paper itself

Abstract

Hearing loss and balance disorders affect millions of people worldwide. Sensory transduction in the inner ear requires both mechanosensory hair cells (HCs) and surrounding glia-like supporting cells (SCs). HCs are susceptible to death from aging, noise overexposure, and treatment with therapeutic drugs that have ototoxic side effects; these ototoxic drugs include the aminoglycoside antibiotics and the antineoplastic drug cisplatin. Although both classes of drugs are known to kill HCs, their effects on SCs are less well understood. Recent data indicate that SCs sense and respond to HC stress, and that their responses can influence HC death, survival, and phagocytosis. These responses to HC stress and death are critical to the health of the inner ear. Here we have used live confocal imaging of the adult mouse utricle, to examine the SC responses to HC death caused by aminoglycosides or cisplatin. Our data indicate that when HCs are killed by aminoglycosides, SCs efficiently remove HC corpses from the sensory epithelium in a process that includes constricting the apical portion of the HC after loss of membrane integrity. SCs then form a phagosome, which can completely engulf the remaining HC body, a phenomenon not previously reported in mammals. In contrast, cisplatin treatment results in accumulation of dead HCs in the sensory epithelium, accompanied by an increase in SC death. The surviving SCs constrict fewer HCs and display impaired phagocytosis. These data are supported by in vivo experiments, in which cochlear SCs show reduced capacity for scar formation in cisplatin-treated mice compared with those treated with aminoglycosides. Together, these data point to a broader defect in the ability of the cisplatin-treated SCs, to preserve tissue health in the mature mammalian inner ear.

Indexed as

AnimalsAntibiotics, AntineoplasticApoptosisCells, CulturedCell SurvivalCisplatinFemaleMaleMiceMice, Inbred CBAMicroscopy, ConfocalNeomycinPhagocytosisSaccule and UtricleAntibiotics, AntineoplasticCisplatinNeomycin

Identifiers

PMID25929858
PMCPMC4816108
OpenAlexW2080668937

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.