Identification of proteins differentially expressed by glutamate treatment in cerebral cortex of neonatal rats
10.1186/s42826-019-0026-9
- Author:
Ju Bin KANG
1
;
Dong Ju PARK
;
Phil Ok KOH
Author Information
1. Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinju-daero, Jinju 52828, South Korea. pokoh@gnu.ac.kr
- Publication Type:Original Article
- Keywords:
Cerebral cortex;
Glutamate;
Neonate;
Proteomics
- MeSH:
Animals;
Brain;
Cerebral Cortex;
Chaperonin 60;
Electrophoresis, Gel, Two-Dimensional;
Glutamic Acid;
Humans;
Infant, Newborn;
Isocitrate Dehydrogenase;
Mass Spectrometry;
Metabolism;
Neurons;
Peroxiredoxins;
Proteasome Endopeptidase Complex;
Proteolysis;
Proteomics;
Rats;
Rats, Sprague-Dawley;
Signal Transduction;
Thioredoxins;
Ubiquitin Thiolesterase
- From:Laboratory Animal Research
2019;35(4):172-179
- CountryRepublic of Korea
- Language:English
-
Abstract:
Glutamate leads to neuronal cell damage by generating neurotoxicity during brain development. The objective of this study is to identify proteins that differently expressed by glutamate treatment in neonatal cerebral cortex. Sprague-Dawley rat pups (post-natal day 7) were intraperitoneally injected with vehicle or glutamate (10 mg/kg). Brain tissues were isolated 4 h after drug treatment and fixed for morphological study. Moreover, cerebral cortices were collected for protein study. Two-dimensional gel electrophoresis and mass spectrometry were carried out to identify specific proteins. We observed severe histopathological changes in glutamate-exposed cerebral cortex. We identified various proteins that differentially expressed by glutamate exposure. Identified proteins were thioredoxin, peroxiredoxin 5, ubiquitin carboxy-terminal hydrolase L1, proteasome subunit alpha proteins, isocitrate dehydrogenase, and heat shock protein 60. Heat shock protein 60 was increased in glutamate exposed condition. However, other proteins were decreased in glutamate-treated animals. These proteins are related to anti-oxidant, protein degradation, metabolism, signal transduction, and anti-apoptotic function. Thus, our findings can suggest that glutamate leads to neonatal cerebral cortex damage by regulation of specific proteins that mediated with various functions.
