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Estrogen receptor activation contributes to RNF146 expression and neuroprotection in Parkinson's disease models

Title
Estrogen receptor activation contributes to RNF146 expression and neuroprotection in Parkinson's disease models
Authors
Kim, Hyo JungHam, Sang WooLee, Joon YeopJo, AreumLee, Gum HwaLee, Yun SongCho, Myoung LaeShin, Heung MookKim, Dong HoonPletnikova, OlgaTroncoso, Juan CShin, Joo HoLee, Yun IlLee, Yun Jong
DGIST Authors
Lee, Yun Il
Issue Date
2017
Citation
Oncotarget, 8(63), 106721-106739
Type
Article
Article Type
Article
Keywords
estrogen receptorliquiritigeninnicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase 1oxidopamineprotein RNF146ubiquitin protein ligase E3unclassified drugadultagedanimal cellanimal experimentanimal modelanimal tissueArticlecell deathcontrolled studyembryoenzyme activationfemalehigh throughput screeninghumanhuman cellhuman tissuemalemiddle agedmousenonhumanParkinson diseasepathogenesispromoter regionprotein expressionprotein functionSH-SY5Y cell linevery elderly
ISSN
1949-2553
Abstract
RNF146 is an E3 ubiquitin ligase that specifically recognizes and polyubiquitinates poly (ADP-ribose) (PAR)-conjugated substrates for proteasomal degradation. RNF146 has been shown to be neuroprotective against PAR polymerase-1 (PARP1)-induced cell death during stroke. Here we report that RNF146 expression and RNF146 inducers can prevent cell death elicited by Parkinson's disease (PD)-associated and PARP1-activating stimuli. In SH-SY5Y cells, RNF146 expression conferred resistance to toxic stimuli that lead to PARP1 activation. High-throughput screen using a luciferase construct harboring the RNF146 promoter identified liquiritigenin as an RNF146 inducer. We found that RNF146 expression by liquiritigenin was mediated by estrogen receptor activation and contributed to cytoprotective effect of liquiritigenin. Finally, RNF146 expression by liquiritigenin in mouse brains provided dopaminergic neuroprotection in a 6-hydroxydopamine PD mouse model. Given the presence of PARP1 activity and RNF146 deficits in PD, it could be a potential therapeutic strategy to restore RNF146 expression by natural compounds or estrogen receptor activation. © Kim et al.
URI
http://hdl.handle.net/20.500.11750/5662
DOI
10.18632/oncotarget.21828
Publisher
Impact Journals LLC
Related Researcher
Files:
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Collection:
Well Aging Research Center1. Journal Articles


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