Evidence map›Paper›PMID 35204073›Full record

ArticleAntioxidants (Basel, Switzerland)2022

Protective Effect of GIP against Monosodium Glutamate-Induced Ferroptosis in Mouse Hippocampal HT-22 Cells through the MAPK Signaling Pathway.

Jiwon Ko, Soyoung Jang, Wookbong Kwon, Si-Yong Kim, Soyeon Jang, Eungyung Kim, Young-Rae Ji, Sijun Park, Myoung-Ok Kim, Seong-Kyoon Choi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2022. 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
2.9field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

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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

14 authors at 3 institutions in 2 countries.

Jiwon KoBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.ORCID 0000-0003-2034-6730
Soyoung JangBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.
Wookbong KwonCore Protein Resources Center, DGIST, Daegu 42988, Korea.
Si-Yong KimBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.ORCID 0000-0002-9583-8193
Soyeon JangBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.
Eungyung KimDepartment of Animal Science and Biotechnology, Kyungpook National University, Sangju-si 37224, Korea.
Young-Rae JiBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.ORCID 0000-0002-8825-9783
Sijun ParkSchool of Life Science, Kyungpook National University, Daegu 42988, Korea.ORCID 0000-0002-8791-8249
Myoung-Ok KimDepartment of Animal Science and Biotechnology, Kyungpook National University, Sangju-si 37224, Korea.
Seong-Kyoon ChoiCore Protein Resources Center, DGIST, Daegu 42988, Korea.
Dong-Hyung ChoBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.
Hyun-Shik LeeBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.ORCID 0000-0002-3837-9867
Su-Geun LimSchool of Life Science, Kyungpook National University, Daegu 42988, Korea.ORCID 0000-0001-5433-2498
Zae-Young RyooBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.
Kyungpook National University · KRDaegu Gyeongbuk Institute of Science and Technology · KRNational Institutes of Health · US

Funding

National Research Foundation of Korea 2020R1A4A1018280National Research Foundation of Korea 2020R1I1A1A01074542National Research Foundation of Korea 2020R1l1A2075315National Research Foundation of Korea 2021R1I1A1A0105962311
6 · The paper itself

Abstract

The effect of glucose-dependent insulinotropic polypeptide (GIP) on cells under oxidative stress induced by glutamate, a neurotransmitter, and the underlying molecular mechanisms were assessed in the present study. We found that in the pre-treatment of HT-22 cells with glutamate in a dose-dependent manner, intracellular ROS were excessively generated, and additional cell damage occurred in the form of lipid peroxidation. The neurotoxicity caused by excessive glutamate was found to be ferroptosis and not apoptosis. Other factors (GPx-4, Nrf2, Nox1 and Hspb1) involved in ferroptosis were also identified. In other words, it was confirmed that GIP increased the activity of sub-signalling molecules in the process of suppressing ferroptosis as an antioxidant and maintained a stable cell cycle even under glutamate-induced neurotoxicity. At the same time, in HT-22 cells exposed to ferroptosis as a result of excessive glutamate accumulation, GIP sustained cell viability by activating the mitogen-activated protein kinase (MAPK) signalling pathway. These results suggest that the overexpression of the GIP gene increases cell viability by regulating mechanisms related to cytotoxicity and reactive oxygen species production in hippocampal neuronal cell lines.

Indexed as

cellular oxidative homeostasisferroptosisglucose-dependent insulinotropic polypeptidemitogen-activated protein kinasemonosodium glutamatemouse hippocampal HT-22 cellsneurotoxicityoxidative stress

Identifiers

PMID35204073
PMCPMC8868324
OpenAlexW4205862074

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.