Evidence map›Paper›PMID 31861721›Full record

ArticleCells2019

Peroxiredoxin 5 Silencing Sensitizes Dopaminergic Neuronal Cells to Rotenone via DNA Damage-Triggered ATM/p53/PUMA Signaling-Mediated Apoptosis.

Mei-Jen Wang, Hsin-Yi Huang, Tsung-Lang Chiu, Hui-Fen Chang, Hsin-Rong Wu

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. DNA Damage-Mediated Neurotoxicity in Parkinson's Disease.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Evaluation of biomarkers in liver followingJournal of diabetes and metabolic disorders · 2020
    Article
  16. Peroxiredoxins in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2020
    Review
  17. 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 at 2 institutions in 1 country.

Mei-Jen WangDepartment of Medical Research, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan.
Hsin-Yi HuangDepartment of Medical Research, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan.
Tsung-Lang ChiuDivision of Neurosurgery, Neuro-Medical Scientific Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan.
Hui-Fen ChangDepartment of Medical Research, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan.
Hsin-Rong WuDepartment of Medical Research, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan.
Hualien Tzu Chi Medical Center · TWTzu Chi University · TW

Funding

Buddhist Tzu Chi Medical Foundation, Taiwan TCMFRP-106-01-02Hualien Tzu Chi Hospital, Taiwan TCRD105-33 and TCRD106-41Ministry of Science and Technology, Taiwan MOST 105-2320-B-303-002-MY3
6 · The paper itself

Abstract

Peroxiredoxins (Prxs) are a family of thioredoxin peroxidases. Accumulating evidence suggests that changes in the expression of Prxs may be involved in neurodegenerative diseases pathology. However, the expression and function of Prxs in Parkinson's disease (PD) remains unclear. Here, we showed that Prx5 was the most downregulated of the six Prx subtypes in dopaminergic (DA) neurons in rotenone-induced cellular and rat models of PD, suggesting possible roles in regulating their survival. Depletion of Prx5 sensitized SH-SY5Y DA neuronal cells to rotenone-induced apoptosis. The extent of mitochondrial membrane potential collapse, cytochrome c release, and caspase activation was increased by Prx5 loss. Furthermore, Prx5 knockdown enhanced the induction of PUMA by rotenone through a p53-dependent mechanism. Using RNA interference approaches, we demonstrated that the p53/PUMA signaling was essential for Prx5 silencing-exacerbated mitochondria-driven apoptosis. Additionally, downregulation of Prx5 augmented rotenone-induced DNA damage manifested as induction of phosphorylated histone H2AX (γ-H2AX) and activation of ataxia telangiectasia mutated (ATM) kinase. The pharmacological inactivation of ATM revealed that ATM was integral to p53 activation by DNA damage. These findings provided a novel link between Prx5 and DNA damage-triggered ATM/p53/PUMA signaling in a rotenone-induced PD model. Thus, Prx5 might play an important role in protection against rotenone-induced DA neurodegeneration.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCells, CulturedCell SurvivalDisease Models, AnimalDNA DamageDopaminergic NeuronsDrug SynergismGene Knockdown TechniquesHumansMaleParkinson DiseasePeroxiredoxinsPrimary Cell CultureRatsRotenoneAtaxia Telangiectasia Mutated ProteinsPeroxiredoxinsPRDX5 protein, humanPrdx5 protein, ratRotenoneTumor Suppressor Protein p53Tumor Suppressor ProteinsATMDNA damagedopaminergic neuronsP53Parkinson’s diseaseperoxiredoxin 5PUMArotenoneγ-H2AX

Identifiers

PMID31861721
PMCPMC7016837
OpenAlexW2995894883

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.