Evidence map›Paper›PMID 41327786›Full record

ArticleRedox report : communications in free radical research2025

Dynamic redox monitoring in differentiated human neuroblastoma models of Parkinson's disease.

Jungeun Lim, Xavier Zhou, Srija Pamujula, Rukkia Liaqat, Ananya Achanta, Loren Looger, Benjamin C Campbell, Melissa M Campbell

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox report : communications in free radical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. 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.

Jungeun LimDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, USA.ORCID 0000-0002-2961-2348
Xavier ZhouDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, USA.
Srija PamujulaDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, USA.
Rukkia LiaqatDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, USA.
Ananya AchantaDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, USA.
Loren LoogerDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, USA.ORCID 0000-0002-7531-1757
Benjamin C CampbellDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, USA.ORCID 0000-0001-8041-5561
Melissa M CampbellDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, USA.ORCID 0000-0002-6265-8882

Funding

UC San Diego FIRST ProgramU54CA272220 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MARIA ELENA MARTINEZ, Joann Trejo · 2022 to 2026
$21.2M
NCI NIH HHS U54 CA272220
6 · The paper itself

Abstract

backgroundOxidative stress plays a critical role in the degeneration of midbrain dopaminergic (DA) neurons in Parkinson's disease (PD). However, therapies targeting redox mechanisms are hindered by a lack of scalable and inexpensive redox-focused preclinical models.

methodsWe stably expressed the glutathione-specific redox-sensitive fluorescent protein Grx-roGFP2 in SH-SY5Y and BE(2)-M17 neuroblastoma cell lines. We developed an improved differentiation protocol using staurosporine and dbcAMP to enhance dopaminergic-like characteristics, assessed by DA marker expression, and characterized responses to PD-relevant toxins.

resultsBE(2)-M17 cells expressed higher DA markers than SH-SY5Y cells, and the improved protocol further increased DA markers. Differentiated neuroblastoma cells with dopaminergic-like features showed greater sensitivity to MPP+ and paraquat, with reduced viability, increased oxidative stress, glutathione oxidation, decreased TH expression, and altered neuronal morphology, paralleling patterns observed in PD-related oxidative injury. roGFP2 enabled robust, real-time redox monitoring, correlating oxidative stress with phenotype. Sublethal toxin exposure caused mitochondrial alterations and redox shifts. Pretreatment with N-acetyl-L-cysteine (NAC) mitigated oxidative stress, improved viability, and partially restored TH expression and morphology.

conclusionThis neuroblastoma-based model with dopaminergic-like features enables scalable, real-time redox monitoring and detailed phenotypic analyses. It expands access to redox biology platforms for investigating neurodegeneration and evaluating antioxidant therapeutic strategies relevant to neurodegeneration.

Indexed as

NeuroblastomaParkinson DiseaseCell DifferentiationCell Line, TumorCell SurvivalDopaminergic NeuronsGlutathioneHumansOxidation-ReductionOxidative StressGlutathionedopaminergic neuronsneurotoxicologyoxidative stressParkinson’s diseaseredox sensor

Identifiers

PMID41327786
PMCPMC12671422

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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.