Evidence map›Paper›PMID 28349361›Full record

ArticleNeurochemical research2017

Transient Cerebral Ischemia Alters GSK-3β and p-GSK-3β Immunoreactivity in Pyramidal Neurons and Induces p-GSK-3β Expression in Astrocytes in the Gerbil Hippocampal CA1 Area.

Bai Hui Chen, Ji Hyeon Ahn, Joon Ha Park, Bich Na Shin, Yun Lyul Lee, Il Jun Kang, Seongkweon Hong, Yang Hee Kim, Yong Hwan Jeon, In Hye Kim and 6 more

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Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

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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

16 authors.

Bai Hui ChenDepartment of Histology and Embryology, Institute of Neuroscience, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, People's Republic of China.
Ji Hyeon AhnDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, 24252, South Korea.
Joon Ha ParkDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, 24252, South Korea.
Bich Na ShinDepartment of Physiology, College of Medicine, and Institute of Neurodegeneration and Neuroregeneration, Hallym University, Chuncheon, 24252, South Korea.
Yun Lyul LeeDepartment of Physiology, College of Medicine, and Institute of Neurodegeneration and Neuroregeneration, Hallym University, Chuncheon, 24252, South Korea.
Il Jun KangDepartment of Food Science and Nutrition, Hallym University, Chuncheon, 24252, South Korea.
Seongkweon HongDepartment of Surgery, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea.
Yang Hee KimDepartment of Surgery, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea.
Yong Hwan JeonDepartment of Radiology, School of Medicine, Kangwon National University, Chuncheon, 24289, South Korea.
In Hye KimDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea.
Jeong Hwi ChoDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea.
Tae-Kyeong LeeDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea.
Jae Chul LeeDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea.
Moo-Ho WonDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea. mhwon@kangwon.ac.kr.
Jun Hwi ChoDepartment of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea.
Joong Bum MoonDepartment of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea. zammanza@kangwon.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen synthase kinase 3β (GSK-3β) is a key downstream protein in the PI3K/Akt pathway. Phosphorylation of serine 9 of GSK-3β (GSK-3β activity inhibition) promotes cell survival. In this study, we examined changes in expressions of GSK-3β and phosphorylation of GSK-3β (p-GSK-3β) in the gerbil hippocampal CA1 area after 5 min of transient cerebral ischemia. GSK-3β immunoreactivity in the CA1 area was increased in pyramidal cells at 6 h after ischemia-reperfusion. It was decreased in CA1 pyramidal cells from 12 h after ischemia-reperfusion, and hardly detected in the CA1 pyramidal cells at 5 days after ischemia-reperfusion. p-GSK-3β immunoreactivity was slightly decreased in CA1 pyramidal cells at 6 and 12 h after ischemia-reperfusion. It was significantly increased in these cells at 1 and 2 days after ischemia-reperfusion. Five days after ischemia-reperfusion, p-GSK-3β immunoreactivity was hardly found in CA1 pyramidal cells. However, p-GSK-3β immunoreactivity was strongly expressed in astrocytes primarily distributed in strata oriens and radiatum. In conclusion, GSK-3β and p-GSK-3β were significantly changed in pyramidal cells and/or astrocytes in the gerbil hippocampal CA1 area following 5 min of transient cerebral ischemia. This finding indicates that GSK-3β and p-GSK-3β are closely related to delayed neuronal death.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsAstrocytesAvoidance LearningBrain IschemiaCA1 Region, HippocampalCell DeathGerbillinaeGlycogen Synthase Kinase 3 betaMalePyramidal CellsGlycogen Synthase Kinase 3 betaAstrocyteGlycogen synthase kinaseHippocampal CA1 areaIschemia–reperfusion injuryPhosphoinositide-3-kinase/Akt pathwayPyramidal cell

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Registered trials

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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.