Identification of proteins differentially expressed by glutamate treatment in cerebral cortex of neonatal rats

Kang, Ju-Bin; Park, Dong-Ju; Koh, Phil-Ok

doi:10.1186/s42826-019-0026-9

Cited by 5 publications

(6 citation statements)

References 37 publications

(36 reference statements)

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“…We previously showed that glutamate exposure induces neuronal cell damage in neonates by up-and down-regulation of specific proteins (Kang et al, 2019). Damaged neurons with atypical round shapes and shrunken dendrites were found in cells from the glutamate-treated cerebral cortex [14]. The number of anomalous neurons was increased by glutamate exposure.…”

Section: Discussionmentioning

confidence: 94%

“…Moreover, glutamate increases intracellular calcium levels and induces mitochondrial dysfunction [16]. We previously showed that glutamate exposure induces neuronal cell damage in neonates by up-and down-regulation of specific proteins (Kang et al, 2019). Damaged neurons with atypical round shapes and shrunken dendrites were found in cells from the glutamate-treated cerebral cortex [14].…”

Section: Discussionmentioning

confidence: 98%

“…However, phosphorylated Bcl-2 associated death promoter (Bad) interacts with 14-3-3 and inactivates its pro-apoptotic function [13]. Our previous study demonstrated that glutamate exposure induces neonatal cerebral cortex damage by modulating a variety of proteins [14]. We propose that glutamate exposure causes neuronal cell death by regulating 14-3-3 proteins during brain development.…”

Section: Introductionmentioning

confidence: 98%

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Decrease of 14–3-3 proteins by glutamate exposure in the cerebral cortex of newborn rats

et al. 2020

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Glutamate is a representative excitatory neurotransmitter. However, excessive glutamate exposure causes neuronal cell damage by generating neuronal excitotoxicity. Excitotoxicity in neonates caused by glutamate treatment induces neurological deficits in adults. The 14-3-3 family proteins are conserved proteins that are expressed ubiquitously in a variety of tissues. These proteins contribute to cellular processes, including signal transduction, protein synthesis, and cell cycle control. We proposed that glutamate induces neuronal cell damage by regulating 14-3-3 protein expression in newborn animals. In this study, we investigated the histopathological changes and 14-3-3 proteins expressions as a result of glutamate exposure in the neonatal cerebral cortex. Rat pups at post-natal day 7 were intraperitoneally administrated with vehicle or glutamate (10 mg/kg). Animals were sacrificed 4 h after treatment, and brain tissues were fixed for histological study. Cerebral cortices were isolated and frozen for proteomic study. We observed serious histopathological damages including shrunken dendrites and atypical neurons in glutamate-treated cerebral cortices. In addition, we identified that 14-3-3 family proteins decreased in glutamate-exposed cerebral cortices using a proteomic approach. Moreover, Western blot analysis provided results that glutamate treatment in neonates decreased 14-3-3 family proteins expressions, including the β/α, ζ/δ, γ, ε, τ, and η isoforms. 14-3-3 proteins are involved in signal transduction, metabolism, and anti-apoptotic functions. Thus, our findings suggest that glutamate induces neonatal neuronal cell damage by modulating 14-3-3 protein expression.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 98%

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Decrease of 14–3-3 proteins by glutamate exposure in the cerebral cortex of newborn rats

et al. 2020

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“…MCAO damage induces reduction of proteasome subunit alpha types 1 and 3, and retinoic acid alleviates decreases in these proteins. We previously showed decrease of proteasome subunit alpha in glutamateexposed cerebral cortex [45]. Decrease of these proteins is involved in cerebral cortex damage during neuronal development [45].…”

Section: Discussionmentioning

confidence: 95%

Retinoic acid regulates the ubiquitin–proteasome system in a middle cerebral artery occlusion animal model

et al. 2022

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Background Retinoic acid is a major metabolite of vitamin A and exerts beneficial effects including anti-oxidant and anti-inflammatory activities in neurons. The ubiquitin–proteasome system is an important biological system that regulates cell survival. Ubiquitination regulates protein degradation and plays an important role in oxidative stress. Deubiquitinating enzymes cleave ubiquitin from proteins and control ubiquitination-induced degradation. We detected decreases in ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in cerebral ischemic damage. In this study, we investigated whether retinoic acid regulates the expression of deubiquitinating enzymes ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in cerebral ischemic injury. Right middle cerebral artery occlusion (MCAO) was performed to induce cerebral ischemic damage in male rats. Retinoic acid (5 mg/kg) or vehicle was intraperitoneally injected every day from 4 days before surgery. Neurological behavioral tests were performed 24 h after MCAO, and right cerebral cortical tissues were collected. Results MCAO damage caused neurological behavioral dysfunction, and retinoic acid alleviated these deficits. The identified proteins decreased in MCAO animals with vehicle, while retinoic acid treatment attenuated these decreases. The results of proteomic study were confirmed by a reverse transcription-PCR technique. Expressions of ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 were decreased in MCAO animals treated with vehicle. Retinoic acid treatment alleviated these MCAO-induced reductions. The ubiquitin–proteasome system plays an essential role in maintaining cell function and preserving cell shape against ischemic damage. Conclusions These findings suggest that retinoic acid regulates ubiquitin- and proteasome-related proteins including ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in a brain ischemia model. Changes in these proteins are involved in the neuroprotective effects of retinoic acid.

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“…Therefore, PP2A subunit B is considered an important factor in maintaining neurobiological function. We have previously shown that glutamate exposure causes neonatal cerebral cortical damage by regulating various proteins [15]. We assume that glutamate exposure controls the PP2A subunit B protein during brain development, causing neuronal damage.…”

Section: Introductionmentioning

confidence: 98%

Decrease of protein phosphatase 2A subunit B by glutamate exposure in the cerebral cortex of neonatal rats

et al. 2020

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Glutamate induces neurotoxicity during brain development, causing nerve damage. Protein phosphatase 2A (PP2A) is a type of serine/threonine phosphatase that regulates various biological functions. Among the PP2A subunit types, subunit B is abundant in brain tissue and plays an essential role in the nervous system. This study investigated changes in PP2A subunit B expression through glutamate exposure in the cerebral cortex of newborn rats. Sprague-Dawley rat pups (7 days after birth) were injected intraperitoneally with vehicle or glutamate (10 mg/kg). After 4 h of drug treatment, the brain tissue was isolated and fixed for morphological study. In addition, the cerebral cortex was collected for RNA and protein works. We observed severe histopathological changes including swollen neuron and atrophied dendrite in the glutamate exposed cerebral cortex. Glutamate exposure leads to a decrease in PP2A subunit B. Reverse-transcription PCR and Western blot analyses confirmed that glutamate induces a decrease of PP2A subunit B in the cerebral cortex of newborn rats. Moreover, immunohistochemical study showed a decrease in PP2A subunit B positive cells. The reduction of PP2A subunit B expression is considered an indicator of neurodegenerative damage. These results suggest that glutamate exposure causes neuronal damage in the cerebral cortex of new born rats through a decrease in PP2A subunit B.

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Identification of proteins differentially expressed by glutamate treatment in cerebral cortex of neonatal rats

Cited by 5 publications

References 37 publications

Decrease of 14–3-3 proteins by glutamate exposure in the cerebral cortex of newborn rats

Decrease of 14–3-3 proteins by glutamate exposure in the cerebral cortex of newborn rats

Retinoic acid regulates the ubiquitin–proteasome system in a middle cerebral artery occlusion animal model

Decrease of protein phosphatase 2A subunit B by glutamate exposure in the cerebral cortex of neonatal rats

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