Evidence map›Paper›PMID 30191426›Full record

ArticleJournal of the Association for Research in Otolaryngology : JARO2018

The Stress Response in the Non-sensory Cells of the Cochlea Under Pathological Conditions-Possible Role in Mediating Noise Vulnerability.

Anni Herranen, Kuu Ikäheimo, Jussi Virkkala, Ulla Pirvola

Abstract read
In one paragraph

Article in Journal of the Association for Research in Otolaryngology : JARO, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Pharmacological Approaches to Hearing Loss.Pharmacological reviews · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. KSR1 Knockout Mouse Model Demonstrates MAPK Pathway's Key Role in Cisplatin- and Noise-induced Hearing Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  9. Review
  10. Article
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  12. Article
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  14. 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

4 authors at 2 institutions in 1 country.

Anni HerranenMolecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Viikinkaari 1, P.O. Box 65, 00014, Helsinki, Finland.
Kuu IkäheimoMolecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Viikinkaari 1, P.O. Box 65, 00014, Helsinki, Finland.
Jussi VirkkalaFinnish Institute of Occupational Health, 00251, Helsinki, Finland.
Ulla PirvolaMolecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Viikinkaari 1, P.O. Box 65, 00014, Helsinki, Finland. ulla.pirvola@helsinki.fi.ORCID 0000-0001-5285-4225
University of Helsinki · FIFinnish Institute of Occupational Health · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various stressors, such as loud sounds and the effects of aging, impair the function and viability of the cochlear sensory cells, the hair cells. Stressors trigger pathophysiological changes in the cochlear non-sensory cells as well. We have here studied the stress response mounted in the lateral wall of the cochlea during acute noise stress and during age-related chronic stress. We have used the activation of JNK/c-Jun, ERK, and NF-κB pathways as a readout of the stress response, and the expression of the FoxO3 transcription factor as a possible additional player in cellular stress. In the aging cochlea, NF-κB transcriptional activity was strongly induced in the stria vascularis of the lateral wall. This induction was linked with the atrophy of the stria vascularis, suggesting a role for NF-κB signaling in mediating age-related strial degeneration. Acutely following noise exposure, the JNK/c-Jun, ERK, and NF-κB pathways were activated in the spiral ligament of the lateral wall of CBA/Ca mice. This activation was concomitant with the morphological transformation of macrophages, suggesting that the upregulation of stress signaling leads to macrophage activation. In contrast, C57BL/6J mice lacked these responses. Only the combination of noise exposure and a systemic stressor, lipopolysaccharide, exceeded the threshold for the activation of stress signaling in the lateral wall of C57BL/6J mice. In addition, we found that, at the young adult age, outer hair cells of CBA/Ca mice are much more vulnerable to loud sounds compared to these cells of C57BL/6J mice. These results suggest that the differential stress response in the lateral wall of the two mouse strains underlies, in part, the differential noise vulnerability of their outer hair cells. Together, we propose that the molecular stress response in the lateral wall modulates the outcome of the stressed cochlea.

Indexed as

Stress, PhysiologicalAgingAnimalsCochleaForkhead Box Protein O3LipopolysaccharidesMAP Kinase Signaling SystemMice, Inbred C57BLMice, Inbred CBAMice, TransgenicNF-kappa BNoiseProto-Oncogene Proteins c-junForkhead Box Protein O3FoxO3 protein, mouseLipopolysaccharidesNF-kappa BProto-Oncogene Proteins c-junagingauditorylateral wallLPSnoisestress signaling

Identifiers

PMID30191426
PMCPMC6249157
OpenAlexW2890914129

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.