Evidence map›Paper›PMID 31078568›Full record

ArticleExperimental cell research2019

Inhibition of protein nitration prevents cisplatin-induced inactivation of STAT3 and promotes anti-apoptotic signaling in organ of Corti cells.

Rita Rosati, Monazza Shahab, William L Neumann, Samson Jamesdaniel

Open access · greenAbstract read
In one paragraph

Article in Experimental cell research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Inhibition of Gpx4-mediated ferroptosis alleviates cisplatin-induced hearing loss in C57BL/6 mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  8. Article
  9. Genes · 2023
    Article
  10. Nitrative Stress and Auditory Dysfunction.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Fundamental Mechanisms of the Cell Death Caused by Nitrosative Stress.Frontiers in cell and developmental biology · 2021
    Review
  15. Review
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.

Rita RosatiInstitute of Environmental Health Sciences, Wayne State University, Detroit, MI, USA.
Monazza ShahabInstitute of Environmental Health Sciences, Wayne State University, Detroit, MI, USA.
William L NeumannDepartment of Pharmaceutical Sciences, Southern Illinois University Edwardsville, Edwardsville, IL, USA.
Samson JamesdanielInstitute of Environmental Health Sciences, Wayne State University, Detroit, MI, USA; Department of Family Medicine and Public Health Sciences, Wayne State University, Detroit, MI, USA. Electronic address: sjamesdaniel@wayne.edu.
Wayne State University · USSouthern Illinois University Edwardsville · US

Funding

Pilot Project ProgramP30ES020957 · NIEHS · WAYNE STATE UNIVERSITY · PI RUNGE-MORRIS, MELISSA A · 2014 to 2021
$10.1M
NovaSeq Shared Instrumentation Grant for Wayne State UniversityS10OD025170 · OD · WAYNE STATE UNIVERSITY · PI RUDEN, DOUGLAS M · 2018 to 2018
$600k
Heavy metal exposure, genetic predisposition, and auditory dysfunction: A cross-sectional study in a high-risk urban cohortK01ES028750 · NIEHS · WAYNE STATE UNIVERSITY · PI JAMESDANIEL, SAMSON · 2018 to 2020
$394k
NIEHS NIH HHS K01 ES028750NIEHS NIH HHS P30 ES020957NIH HHS S10 OD025170
6 · The paper itself

Abstract

JAK/STAT pathway is one among the several oxidative stress-responsive signaling pathways that play a critical role in facilitating cisplatin-induced ototoxicity. Cisplatin treatment decreases the levels of cochlear LMO4, which acts as a scaffold for IL6-GP130 protein complex. Cisplatin-induced nitration and degradation of LMO4 could destabilize this protein complex, which in turn could compromise the downstream STAT3-mediated cellular defense mechanism. Here, we investigated the link between cisplatin-induced nitrative stress and STAT3-mediated apoptosis by using organ of Corti cell cultures. SRI110, a peroxynitrite decomposition catalyst that prevented cisplatin-induced decrease in LMO4 levels and ototoxicity, was used to inhibit nitrative stress. Immunoblotting and immunostaining indicated that cisplatin treatment decreased the expression levels, phosphorylation, and nuclear localization of STAT3 in UB/OC1 cells. Inhibition of nitration by SRI110 co-treatment prevented cisplatin-induced inactivation of STAT3 and promoted its nuclear localization. SRI110 co-treatment reversed the cisplatin-induced changes in the expression levels of Bcl2l1, Ccnd1, Jak2, Jak3, and Src and significantly attenuated the changes in the expression levels of Cdkn1a, Egfr, Fas, Il6st, Jak1, Stat3, and Tyk2. Collectively, these results suggest that the inhibition of cisplatin-induced nitration prevents the inactivation of STAT3, which in turn enables the transcription of anti-apoptotic genes and thereby helps to mitigate cisplatin-induced toxicity.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCatalysisCell LineCisplatinJanus Kinase 1MiceNitric OxideOrgan of CortiPhosphorylationSignal TransductionSTAT3 Transcription FactorTyrosine3-nitrotyrosineAntineoplastic AgentsCisplatinJak1 protein, mouseJanus Kinase 1Nitric OxideSTAT3 protein, humanSTAT3 Transcription FactorTyrosineCisplatinCochleaLMO4Nitrative stressOtotoxicitySTAT3

Identifiers

PMID31078568
PMCPMC6546436
OpenAlexW2944787790

What OpenQuestion holds

Textmetadata
LicenceTDM
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.