Upregulation of Glutaredoxin 2 alleviates oxygen-glucose deprivation/reoxygenation-induced apoptosis and ROS production in neurons by enhancing Nrf2 signaling via modulation of GSK-3β.
Identifieur interne : 000003 ( Main/Exploration ); précédent : 000002; suivant : 000004Upregulation of Glutaredoxin 2 alleviates oxygen-glucose deprivation/reoxygenation-induced apoptosis and ROS production in neurons by enhancing Nrf2 signaling via modulation of GSK-3β.
Auteurs : Jian Wen [République populaire de Chine] ; Xin Li [République populaire de Chine] ; Shaohua Zheng [République populaire de Chine] ; Ying Xiao [République populaire de Chine]Source :
- Brain research [ 1872-6240 ] ; 2020.
Abstract
Glutaredoxin 2 (GRX2) is an antioxidative protein that exerts a key role in various pathological processes. However, whether GRX2 participates in modulating the oxidative stress during cerebral ischemia/reperfusion, injury is undermined. This study aimed to determine the potential role of GRX2 in regulating oxidative stress in cultured neurons induced by oxygen-glucose deprivation/reoxygenation (OGD/R), a cellular model for study of cerebral ischemia/reperfusion injury in vitro. Here, we showed that GRX2 expression was decreased in neurons subjected to OGD/R exposure. The upregulation of GRX2 markedly improved the viability of OGD/R-exposed neurons and caused a marked reduction in OGD/R-induced apoptosis and reactive oxygen species (ROS) production. On the contrary, depletion of GRX2 exacerbated the OGD/R-induced apoptosis and ROS production in cultured neurons. Moreover, GRX2 upregulation increased nuclear expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and enhanced the activation of Nrf2/ARE signaling associated with modulation of glycogen synthase kinase-3β (GSK-3β) inhibition. Notably, inhibition of Nrf2 markedly abrogated GRX2-mediated protection against OGD/R-induced apoptosis and oxidative stress. Overall, these findings elucidate that GRX2 plays an essential role in regulating the protection against OGD/R-induced apoptosis and oxidative stress in neurons associated with its ability to enhance the activation of Nrf2 via modulation of GSK-3β. Our study indicates that GRX2 may play a key role in modulating neuronal apoptosis and oxidative stress induced by cerebral ischemia/reperfusion injury.
DOI: 10.1016/j.brainres.2020.146946
PubMed: 32522629
Affiliations:
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Electronic address: xiaoyingxy0007@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061</wicri:regionArea><wicri:noRegion>Xi'an 710061</wicri:noRegion></affiliation></author></analytic><series><title level="j">Brain research</title><idno type="eISSN">1872-6240</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glutaredoxin 2 (GRX2) is an antioxidative protein that exerts a key role in various pathological processes. However, whether GRX2 participates in modulating the oxidative stress during cerebral ischemia/reperfusion, injury is undermined. This study aimed to determine the potential role of GRX2 in regulating oxidative stress in cultured neurons induced by oxygen-glucose deprivation/reoxygenation (OGD/R), a cellular model for study of cerebral ischemia/reperfusion injury in vitro. Here, we showed that GRX2 expression was decreased in neurons subjected to OGD/R exposure. The upregulation of GRX2 markedly improved the viability of OGD/R-exposed neurons and caused a marked reduction in OGD/R-induced apoptosis and reactive oxygen species (ROS) production. On the contrary, depletion of GRX2 exacerbated the OGD/R-induced apoptosis and ROS production in cultured neurons. Moreover, GRX2 upregulation increased nuclear expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and enhanced the activation of Nrf2/ARE signaling associated with modulation of glycogen synthase kinase-3β (GSK-3β) inhibition. Notably, inhibition of Nrf2 markedly abrogated GRX2-mediated protection against OGD/R-induced apoptosis and oxidative stress. Overall, these findings elucidate that GRX2 plays an essential role in regulating the protection against OGD/R-induced apoptosis and oxidative stress in neurons associated with its ability to enhance the activation of Nrf2 via modulation of GSK-3β. Our study indicates that GRX2 may play a key role in modulating neuronal apoptosis and oxidative stress induced by cerebral ischemia/reperfusion injury.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">32522629</PMID><DateRevised><Year>2020</Year><Month>07</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-6240</ISSN><JournalIssue CitedMedium="Internet"><Volume>1745</Volume><PubDate><Year>2020</Year><Month>Oct</Month><Day>15</Day></PubDate></JournalIssue><Title>Brain research</Title><ISOAbbreviation>Brain Res</ISOAbbreviation></Journal><ArticleTitle>Upregulation of Glutaredoxin 2 alleviates oxygen-glucose deprivation/reoxygenation-induced apoptosis and ROS production in neurons by enhancing Nrf2 signaling via modulation of GSK-3β.</ArticleTitle><Pagination><MedlinePgn>146946</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-8993(20)30302-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.brainres.2020.146946</ELocationID><Abstract><AbstractText>Glutaredoxin 2 (GRX2) is an antioxidative protein that exerts a key role in various pathological processes. However, whether GRX2 participates in modulating the oxidative stress during cerebral ischemia/reperfusion, injury is undermined. This study aimed to determine the potential role of GRX2 in regulating oxidative stress in cultured neurons induced by oxygen-glucose deprivation/reoxygenation (OGD/R), a cellular model for study of cerebral ischemia/reperfusion injury in vitro. Here, we showed that GRX2 expression was decreased in neurons subjected to OGD/R exposure. The upregulation of GRX2 markedly improved the viability of OGD/R-exposed neurons and caused a marked reduction in OGD/R-induced apoptosis and reactive oxygen species (ROS) production. On the contrary, depletion of GRX2 exacerbated the OGD/R-induced apoptosis and ROS production in cultured neurons. Moreover, GRX2 upregulation increased nuclear expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and enhanced the activation of Nrf2/ARE signaling associated with modulation of glycogen synthase kinase-3β (GSK-3β) inhibition. Notably, inhibition of Nrf2 markedly abrogated GRX2-mediated protection against OGD/R-induced apoptosis and oxidative stress. Overall, these findings elucidate that GRX2 plays an essential role in regulating the protection against OGD/R-induced apoptosis and oxidative stress in neurons associated with its ability to enhance the activation of Nrf2 via modulation of GSK-3β. Our study indicates that GRX2 may play a key role in modulating neuronal apoptosis and oxidative stress induced by cerebral ischemia/reperfusion injury.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wen</LastName><ForeName>Jian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zheng</LastName><ForeName>Shaohua</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Ying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, PR China. Electronic address: xiaoyingxy0007@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>06</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Brain Res</MedlineTA><NlmUniqueID>0045503</NlmUniqueID><ISSNLinking>0006-8993</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">GSK-3β</Keyword><Keyword MajorTopicYN="N">Glutaredoxin 2</Keyword><Keyword MajorTopicYN="N">Nrf2</Keyword><Keyword MajorTopicYN="N">OGD/R</Keyword></KeywordList><CoiStatement>Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>03</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>05</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>06</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>6</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>6</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>6</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32522629</ArticleId><ArticleId IdType="pii">S0006-8993(20)30302-4</ArticleId><ArticleId IdType="doi">10.1016/j.brainres.2020.146946</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wen, Jian" sort="Wen, Jian" uniqKey="Wen J" first="Jian" last="Wen">Jian Wen</name></noRegion><name sortKey="Li, Xin" sort="Li, Xin" uniqKey="Li X" first="Xin" last="Li">Xin Li</name><name sortKey="Xiao, Ying" sort="Xiao, Ying" uniqKey="Xiao Y" first="Ying" last="Xiao">Ying Xiao</name><name sortKey="Zheng, Shaohua" sort="Zheng, Shaohua" uniqKey="Zheng S" first="Shaohua" last="Zheng">Shaohua Zheng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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