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Protective Role of Transduced Tat-Thioredoxin1 (Trx1) against Oxidative Stress-Induced Neuronal Cell Death via ASK1-MAPK Signal Pathway

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Abstract
Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H2O2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NE-kappa B, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.
Author(s)
여은지음원식여혜언손은정권현정김대원김덕수조성우박진서한규형이근욱박종국신민재최수영
Issued Date
2021
Type
Article
Keyword
ApoptosisASK1IschemiaProtein therapyROSTat-Trx1
DOI
10.4062/biomolther.2020.154
URI
https://oak.ulsan.ac.kr/handle/2021.oak/7913
https://ulsan-primo.hosted.exlibrisgroup.com/primo-explore/fulldisplay?docid=TN_cdi_kisti_ndsl_JAKO202113759911512&context=PC&vid=ULSAN&lang=ko_KR&search_scope=default_scope&adaptor=primo_central_multiple_fe&tab=default_tab&query=any,contains,Protective%20Role%20of%20Transduced%20Tat-Thioredoxin1%20(Trx1)%20against%20Oxidative%20Stress-Induced%20Neuronal%20Cell%20Death%20via%20ASK1-MAPK%20Signal%20Pathway&offset=0&pcAvailability=true
Publisher
BIOMOLECULES THERAPEUTICS
Location
대한민국
Language
영어
ISSN
1976-9148
Citation Volume
29
Citation Number
3
Citation Start Page
321
Citation End Page
330
Appears in Collections:
Medicine > Medicine
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