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

Other Titles
Retinoic acid regulates the ubiquitin–proteasome system in a middle cerebral artery occlusion animal model
Authors
강주빈Murad-Ali Shah박동주고필옥
Issue Date
May-2022
Publisher
한국실험동물학회
Keywords
Cerebral ischemia; Neuroprotection; Retinoic acid; Ubiquitin–proteasome system
Citation
Laboratory Animal Research, v.38, no.2, pp.99 - 109
Indexed
KCI
Journal Title
Laboratory Animal Research
Volume
38
Number
2
Start Page
99
End Page
109
URI
https://scholarworks.bwise.kr/gnu/handle/sw.gnu/1291
DOI
10.1186/s42826-022-00123-6
ISSN
1738-6055
Abstract
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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