Evidence map›Paper›PMID 38705005›Full record

ArticleHearing research2024

Quantitative profiling of cochlear synaptosomal proteins in cisplatin-induced synaptic dysfunction.

Monazza Shahab, Rita Rosati, Paul M Stemmer, Alan Dombkowski, Samson Jamesdaniel

Abstract read
In one paragraph

Article in Hearing research, 2024. 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
–field-weighted citation impact
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.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. [Research progress of metalloporphyrin against neurodegene-rative diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Review
  13. 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.

Monazza ShahabDepartment of Pharmacology, Wayne State University, Detroit, MI, USA; Institute of Environment Health Science, Wayne State University, Detroit, MI, USA.
Rita RosatiInstitute of Environment Health Science, Wayne State University, Detroit, MI, USA.
Paul M StemmerInstitute of Environment Health Science, Wayne State University, Detroit, MI, USA.
Alan DombkowskiDepartment of Pediatrics, Wayne State University, Detroit, MI, USA.
Samson JamesdanielDepartment of Pharmacology, Wayne State University, Detroit, MI, USA; Institute of Environment Health Science, Wayne State University, Detroit, MI, USA. Electronic address: sjamesdaniel@wayne.edu.

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
Pilot Project ProgramP30ES020957 · NIEHS · WAYNE STATE UNIVERSITY · PI RUNGE-MORRIS, MELISSA A · 2014 to 2021
$10.1M
Targeting nitrative stress for treatment of cisplatin ototoxicityR01DC020299 · NIDCD · WAYNE STATE UNIVERSITY · PI SAMSON JAMESDANIEL · 2023 to 2026
$1.4M
NCI NIH HHS P30 CA022453NIDCD NIH HHS R01 DC020299NIEHS NIH HHS P30 ES020957
6 · The paper itself

Abstract

The disruption of ribbon synapses in the cochlea impairs the transmission of auditory signals from the cochlear sensory receptor cells to the auditory cortex. Although cisplatin-induced loss of ribbon synapses is well-documented, and studies have reported nitration of cochlear proteins after cisplatin treatment, yet the underlying mechanism of cochlear synaptopathy is not fully understood. This study tests the hypothesis that cisplatin treatment alters the abundance of cochlear synaptosomal proteins, and selective targeting of nitrative stress prevents the associated synaptic dysfunction. Auditory brainstem responses of mice treated with cisplatin showed a reduction in amplitude and an increase in latency of wave I, indicating cisplatin-induced synaptic dysfunction. The mass spectrometry analysis of cochlear synaptosomal proteins identified 102 proteins that decreased in abundance and 249 that increased in abundance after cisplatin treatment. Pathway analysis suggested that the dysregulated proteins were involved in calcium binding, calcium ion regulation, synapses, and endocytosis pathways. Inhibition of nitrative stress by co-treatment with MnTBAP, a peroxynitrite scavenger, attenuated cisplatin-induced changes in the abundance of 27 proteins. Furthermore, MnTBAP co-treatment prevented the cisplatin-induced decrease in the amplitude and increase in the latency of wave I. Together, these findings suggest a potential role of oxidative/nitrative stress in cisplatin-induced cochlear synaptic dysfunction.

Indexed as

CisplatinCochleaHearing LossSynapsesAnimalsEvoked Potentials, Auditory, Brain StemFree Radical ScavengersMaleMass SpectrometryMembrane ProteinsMetalloporphyrinsMice, Inbred StrainsCisplatinFree Radical Scavengersmanganese(III)-tetrakis(4-benzoic acid)porphyrinMembrane ProteinsMetalloporphyrinsCisplatinCochlear synaptosomeMnTBAP chlorideNitrative stressOtotoxicitySynaptic dysfunction

Identifiers

PMID38705005
PMCPMC11116033

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Registered trials

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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.