DJ‐1 modulates the expression of Cu/Zn‐superoxide dismutase‐1 through the Erk1/2–Elk1 pathway in neuroprotection
Identifieur interne : 000348 ( Main/Exploration ); précédent : 000347; suivant : 000349DJ‐1 modulates the expression of Cu/Zn‐superoxide dismutase‐1 through the Erk1/2–Elk1 pathway in neuroprotection
Auteurs : Zhiquan Wang [République populaire de Chine] ; Jun Liu [République populaire de Chine] ; Siyan Chen [République populaire de Chine] ; Ying Wang [République populaire de Chine] ; Li Cao [République populaire de Chine] ; Yu Zhang [République populaire de Chine] ; Wenyan Kang [République populaire de Chine] ; Hui Li [République populaire de Chine] ; Yaxing Gui [République populaire de Chine] ; Shengdi Chen [République populaire de Chine] ; Jianqing Ding [République populaire de Chine]Source :
- Annals of Neurology [ 0364-5134 ] ; 2011-10.
Abstract
Objective:: Loss of function mutations of Park7/DJ‐1 gene increase the susceptibility of dopaminergic cells to reactive oxygen species and cause early onset familial Parkinson disease (PD). However, the mechanisms underlying dopaminergic neuron loss related to DJ‐1 mutation remain undefined. Therefore, it is important to find the new mechanisms underlying the antioxidative functions of DJ‐1. Methods:: DJ‐1 knockdown cells and DJ‐1 knockout mice were used to elucidate the mechanisms underlying the antioxidative stress of DJ‐1. Preliminary study of the saliva from PD patients and controls was used to confirm our findings obtained from the above studies. Results:: Our experiments showed that DJ‐1 interacted with Erk1/2 and was required for the nuclear translocation of Erk1/2 upon oxidative stimulation. The translocation of Erk1/2 activated Elk1 and sequentially promoted superoxide dismutase1 (SOD1) expression. The nuclear translocation of Erk1/2, the activation of Elk1, and the ensuing upregulation of SOD1 were all suppressed in DJ‐1 knockdown cells and DJ‐1 null mice treated with oxidative insult. Furthermore, reintroduction of SOD1 into DJ‐1 knockdown cells protected them against oxidative stress. Finally, in the preliminary study, we found close correlation between the protein levels of DJ‐1 and SOD1 in the saliva samples from different stages of PD patients. Interpretation:: Our studies suggest that DJ‐1 regulates SOD1 expression through Erk1/2–Elk1 pathway in its protective response to oxidative insult. ANN NEUROL 2011
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DOI: 10.1002/ana.22514
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uniqKey="Kang W" first="Wenyan" last="Kang">Wenyan Kang</name></author><author><name sortKey="Li, Hui" sort="Li, Hui" uniqKey="Li H" first="Hui" last="Li">Hui Li</name></author><author><name sortKey="Gui, Yaxing" sort="Gui, Yaxing" uniqKey="Gui Y" first="Yaxing" last="Gui">Yaxing Gui</name></author><author><name sortKey="Chen, Shengdi" sort="Chen, Shengdi" uniqKey="Chen S" first="Shengdi" last="Chen">Shengdi Chen</name></author><author><name sortKey="Ding, Jianqing" sort="Ding, Jianqing" uniqKey="Ding J" first="Jianqing" last="Ding">Jianqing Ding</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:77B4307FAC153306CC0D47A044881E66E433C575</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/ana.22514</idno><idno type="url">https://api.istex.fr/document/77B4307FAC153306CC0D47A044881E66E433C575/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001D78</idno><idno type="wicri:Area/Main/Curation">001A97</idno><idno 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Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Graduate School of the Chinese Academy of Science, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Jun" sort="Liu, Jun" uniqKey="Liu J" first="Jun" last="Liu">Jun Liu</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Siyan" sort="Chen, Siyan" uniqKey="Chen S" first="Siyan" last="Chen">Siyan Chen</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Ying" sort="Wang, Ying" uniqKey="Wang Y" first="Ying" last="Wang">Ying Wang</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Li" sort="Cao, Li" uniqKey="Cao L" first="Li" last="Cao">Li Cao</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Yu" sort="Zhang, Yu" uniqKey="Zhang Y" first="Yu" last="Zhang">Yu Zhang</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Kang, Wenyan" sort="Kang, Wenyan" uniqKey="Kang W" first="Wenyan" last="Kang">Wenyan Kang</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Li, Hui" sort="Li, Hui" uniqKey="Li H" first="Hui" last="Li">Hui Li</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Gui, Yaxing" sort="Gui, Yaxing" uniqKey="Gui Y" first="Yaxing" last="Gui">Yaxing Gui</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Shengdi" sort="Chen, Shengdi" uniqKey="Chen S" first="Shengdi" last="Chen">Shengdi Chen</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Neurodegenerative Diseases, Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Science and Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation><affiliation><wicri:noCountry code="subField">Shanghai 200025 P.R. China</wicri:noCountry></affiliation></author><author><name sortKey="Ding, Jianqing" sort="Ding, Jianqing" uniqKey="Ding J" first="Jianqing" last="Ding">Jianqing Ding</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Neurodegenerative Diseases, Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Science and Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Shanghai</wicri:regionArea><wicri:noRegion>China Shanghai</wicri:noRegion></affiliation><affiliation><wicri:noCountry code="subField">Shanghai 200025 P.R. China</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-10">2011-10</date><biblScope unit="volume">70</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="591">591</biblScope><biblScope unit="page" to="599">599</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">77B4307FAC153306CC0D47A044881E66E433C575</idno><idno type="DOI">10.1002/ana.22514</idno><idno type="ArticleID">ANA22514</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective:: Loss of function mutations of Park7/DJ‐1 gene increase the susceptibility of dopaminergic cells to reactive oxygen species and cause early onset familial Parkinson disease (PD). However, the mechanisms underlying dopaminergic neuron loss related to DJ‐1 mutation remain undefined. Therefore, it is important to find the new mechanisms underlying the antioxidative functions of DJ‐1. Methods:: DJ‐1 knockdown cells and DJ‐1 knockout mice were used to elucidate the mechanisms underlying the antioxidative stress of DJ‐1. Preliminary study of the saliva from PD patients and controls was used to confirm our findings obtained from the above studies. Results:: Our experiments showed that DJ‐1 interacted with Erk1/2 and was required for the nuclear translocation of Erk1/2 upon oxidative stimulation. The translocation of Erk1/2 activated Elk1 and sequentially promoted superoxide dismutase1 (SOD1) expression. The nuclear translocation of Erk1/2, the activation of Elk1, and the ensuing upregulation of SOD1 were all suppressed in DJ‐1 knockdown cells and DJ‐1 null mice treated with oxidative insult. Furthermore, reintroduction of SOD1 into DJ‐1 knockdown cells protected them against oxidative stress. Finally, in the preliminary study, we found close correlation between the protein levels of DJ‐1 and SOD1 in the saliva samples from different stages of PD patients. Interpretation:: Our studies suggest that DJ‐1 regulates SOD1 expression through Erk1/2–Elk1 pathway in its protective response to oxidative insult. ANN NEUROL 2011</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wang, Zhiquan" sort="Wang, Zhiquan" uniqKey="Wang Z" first="Zhiquan" last="Wang">Zhiquan Wang</name></noRegion><name sortKey="Cao, Li" sort="Cao, Li" uniqKey="Cao L" first="Li" last="Cao">Li Cao</name><name sortKey="Chen, Shengdi" sort="Chen, Shengdi" uniqKey="Chen S" first="Shengdi" last="Chen">Shengdi Chen</name><name sortKey="Chen, Shengdi" sort="Chen, Shengdi" uniqKey="Chen S" first="Shengdi" last="Chen">Shengdi Chen</name><name sortKey="Chen, Siyan" sort="Chen, Siyan" uniqKey="Chen S" first="Siyan" last="Chen">Siyan Chen</name><name sortKey="Ding, Jianqing" sort="Ding, Jianqing" uniqKey="Ding J" first="Jianqing" last="Ding">Jianqing Ding</name><name sortKey="Ding, Jianqing" sort="Ding, Jianqing" uniqKey="Ding J" first="Jianqing" last="Ding">Jianqing Ding</name><name sortKey="Gui, Yaxing" sort="Gui, Yaxing" uniqKey="Gui Y" first="Yaxing" last="Gui">Yaxing Gui</name><name sortKey="Kang, Wenyan" sort="Kang, Wenyan" uniqKey="Kang W" first="Wenyan" last="Kang">Wenyan Kang</name><name sortKey="Li, Hui" sort="Li, Hui" uniqKey="Li H" first="Hui" last="Li">Hui Li</name><name sortKey="Liu, Jun" sort="Liu, Jun" uniqKey="Liu J" first="Jun" last="Liu">Jun Liu</name><name sortKey="Wang, Ying" sort="Wang, Ying" uniqKey="Wang Y" first="Ying" last="Wang">Ying Wang</name><name sortKey="Wang, Zhiquan" sort="Wang, Zhiquan" uniqKey="Wang Z" first="Zhiquan" last="Wang">Zhiquan Wang</name><name sortKey="Wang, Zhiquan" sort="Wang, Zhiquan" uniqKey="Wang Z" first="Zhiquan" last="Wang">Zhiquan Wang</name><name sortKey="Zhang, Yu" sort="Zhang, Yu" uniqKey="Zhang Y" first="Yu" last="Zhang">Yu Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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