Evidence map›Paper›PMID 37223703›Full record

ArticleHeliyon2023

Protective effects of cell permeable Tat-PIM2 protein on oxidative stress induced dopaminergic neuronal cell death.

Min Jea Shin, Won Sik Eum, Gi Soo Youn, Jung Hwan Park, Hyeon Ji Yeo, Eun Ji Yeo, Hyun Jung Kwon, Eun Jeong Sohn, Lee Re Lee, Na Yeon Kim and 8 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2023. 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
0.5field-weighted citation impact, top 33% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Dihydroquercetin/Taxifolin Inhibits METTL3/mKidney diseases (Basel, Switzerland)
    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

18 authors at 4 institutions in 1 country.

Min Jea ShinDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Won Sik EumDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Gi Soo YounDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Jung Hwan ParkDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Hyeon Ji YeoDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Eun Ji YeoDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Hyun Jung KwonDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Eun Jeong SohnDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Lee Re LeeDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Na Yeon KimDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Su Yeon KwonDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Su Min KimDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Hyo Young JungDepartment of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, Daejeon, 34134, South Korea.
Duk-Soo KimDepartment of Anatomy and BK21 FOUR Project, College of Medicine, Soonchunhyang University, Cheonan-si 31538, South Korea.
Sung-Woo ChoDepartment of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, South Korea.
Oh-Shin KwonSchool of Life Sciences, College of Natural Sciences Kyungpook National University, Taegu 41566, South Korea.
Dae Won KimDepartment of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung 25457, South Korea.
Soo Young ChoiDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, South Korea.
Hallym University · KRGangneung–Wonju National University · KRUlsan College · KRChungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Oxidative stress is considered as one of the main causes of Parkinson's disease (PD), however the exact etiology of PD is still unknown. Although it is known that Proviral Integration Moloney-2 (PIM2) promotes cell survival by its ability to inhibit formation of reactive oxygen species (ROS) in the brain, the precise functional role of PIM2 in PD has not been fully studied yet. Objective: We investigated the protective effect of PIM2 against apoptosis of dopaminergic neuronal cells caused by oxidative stress-induced ROS damage by using the cell permeable Tat-PIM2 fusion protein Methods: Transduction of Tat-PIM2 into SH-SY5Y cells and apoptotic signaling pathways were determined by Western blot analysis. Intracellular ROS production and DNA damage was confirmed by DCF-DA and TUNEL staining. Cell viability was determined by MTT assay. PD animal model was induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and protective effects were examined using immunohistochemistry. Results: Transduced Tat-PIM2 inhibited the apoptotic caspase signaling and reduced the production of ROS induced by 1-methyl-4-phenylpyridinium (MPP Conclusion: These results indicated that Tat-PIM2 markedly inhibited the loss of dopaminergic neurons by reducing ROS damage, suggesting that Tat-PIM2 might be a suitable therapeutic agent for PD.

Indexed as

ApoptosisOxidative stressParkinson's diseaseProtein therapyProtein transductionROSTat-PIM2

Identifiers

PMID37223703
PMCPMC10200856
OpenAlexW4367396471

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.