Contribution of glutaredoxin-1 to Fas s-glutathionylation and inflammation in ethanol-induced liver injury.
Identifieur interne : 000083 ( Main/Exploration ); précédent : 000082; suivant : 000084Contribution of glutaredoxin-1 to Fas s-glutathionylation and inflammation in ethanol-induced liver injury.
Auteurs : Xiaomin Sun [République populaire de Chine] ; Cuilian Ye [République populaire de Chine] ; Qin Deng [République populaire de Chine] ; Jingyu Chen [République populaire de Chine] ; Chunbao Guo [République populaire de Chine]Source :
- Life sciences [ 1879-0631 ] ; 2020.
Abstract
AIMS
The reversible protein S-glutathionylation (PSSG) modification of Fas augments apoptosis, which can be reversed by the cytosolic deglutathionylation enzyme glutaredoxin-1 (Grx1), but its roles in alcoholic liver injury remain unknown. Therefore, the objective of this study was to investigate the impact of genetic ablation of Grx1 on Fas S-glutathionylation (Fas-SSG) in regulating ethanol-induced injury.
MATERIALS AND METHODS
We evaluated the Grx1 activity and oxidative damage, hepatic injury related indicators, Fas-SSG, we also assess the nuclear factor-κB (NF-κB) signaling, its downstream signal, and Akt signaling cascades, Furthermore, the number of Kupffer cells and related proinflammatory cytokines between WT and Grx1- groups after alcohol exposure.
KEY FINDINGS
Ethanol-fed mice had increased Grx1 activity and oxidative damage in the liver. Grx1-deficient mice had more serious liver damage when exposed to ethanol compared to that of wild-type mice, accompanied by increased alanine aminotransferase and aspartate aminotransferase levels, Fas-SSG, cleaved caspase-3 and hepatocyte apoptosis. Grx1 ablation resulted in the suppression of ethanol-induced NF-κB signaling, its downstream signal, and Akt signaling cascades, which are required for protection against Fas-mediated apoptosis. Accordingly, blocking NK-κB prevented Fas-induced apoptosis in WT mice but not Grx1-/- mice. Furthermore, the number of Kupffer cells and related proinflammatory cytokines, including Akt, were lower in Grx1-/- livers than those of the controls.
SIGNIFICANCE
Grx1 is essential for adaptation to alcohol exposure-induced oxidative injury by modulating Fas-SSG and Fas-induced apoptosis.
DOI: 10.1016/j.lfs.2020.118678
PubMed: 33127518
Affiliations:
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Electronic address: chenjingyu@hospital.cqmu.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Department of Ultrasound, Children's Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Guo, Chunbao" sort="Guo, Chunbao" uniqKey="Guo C" first="Chunbao" last="Guo">Chunbao Guo</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China. Electronic address: guochunbao@hospital.cqmu.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author></analytic><series><title level="j">Life sciences</title><idno type="eISSN">1879-0631</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"><p><b>AIMS</b></p><p>The reversible protein S-glutathionylation (PSSG) modification of Fas augments apoptosis, which can be reversed by the cytosolic deglutathionylation enzyme glutaredoxin-1 (Grx1), but its roles in alcoholic liver injury remain unknown. Therefore, the objective of this study was to investigate the impact of genetic ablation of Grx1 on Fas S-glutathionylation (Fas-SSG) in regulating ethanol-induced injury.</p></div><div type="abstract" xml:lang="en"><p><b>MATERIALS AND METHODS</b></p><p>We evaluated the Grx1 activity and oxidative damage, hepatic injury related indicators, Fas-SSG, we also assess the nuclear factor-κB (NF-κB) signaling, its downstream signal, and Akt signaling cascades, Furthermore, the number of Kupffer cells and related proinflammatory cytokines between WT and Grx1- groups after alcohol exposure.</p></div><div type="abstract" xml:lang="en"><p><b>KEY FINDINGS</b></p><p>Ethanol-fed mice had increased Grx1 activity and oxidative damage in the liver. Grx1-deficient mice had more serious liver damage when exposed to ethanol compared to that of wild-type mice, accompanied by increased alanine aminotransferase and aspartate aminotransferase levels, Fas-SSG, cleaved caspase-3 and hepatocyte apoptosis. Grx1 ablation resulted in the suppression of ethanol-induced NF-κB signaling, its downstream signal, and Akt signaling cascades, which are required for protection against Fas-mediated apoptosis. Accordingly, blocking NK-κB prevented Fas-induced apoptosis in WT mice but not Grx1-/- mice. Furthermore, the number of Kupffer cells and related proinflammatory cytokines, including Akt, were lower in Grx1-/- livers than those of the controls.</p></div><div type="abstract" xml:lang="en"><p><b>SIGNIFICANCE</b></p><p>Grx1 is essential for adaptation to alcohol exposure-induced oxidative injury by modulating Fas-SSG and Fas-induced apoptosis.</p></div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">33127518</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0631</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Oct</Month><Day>27</Day></PubDate></JournalIssue><Title>Life sciences</Title><ISOAbbreviation>Life Sci</ISOAbbreviation></Journal><ArticleTitle>Contribution of glutaredoxin-1 to Fas s-glutathionylation and inflammation in ethanol-induced liver injury.</ArticleTitle><Pagination><MedlinePgn>118678</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0024-3205(20)31431-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.lfs.2020.118678</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">The reversible protein S-glutathionylation (PSSG) modification of Fas augments apoptosis, which can be reversed by the cytosolic deglutathionylation enzyme glutaredoxin-1 (Grx1), but its roles in alcoholic liver injury remain unknown. Therefore, the objective of this study was to investigate the impact of genetic ablation of Grx1 on Fas S-glutathionylation (Fas-SSG) in regulating ethanol-induced injury.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">We evaluated the Grx1 activity and oxidative damage, hepatic injury related indicators, Fas-SSG, we also assess the nuclear factor-κB (NF-κB) signaling, its downstream signal, and Akt signaling cascades, Furthermore, the number of Kupffer cells and related proinflammatory cytokines between WT and Grx1- groups after alcohol exposure.</AbstractText><AbstractText Label="KEY FINDINGS" NlmCategory="RESULTS">Ethanol-fed mice had increased Grx1 activity and oxidative damage in the liver. Grx1-deficient mice had more serious liver damage when exposed to ethanol compared to that of wild-type mice, accompanied by increased alanine aminotransferase and aspartate aminotransferase levels, Fas-SSG, cleaved caspase-3 and hepatocyte apoptosis. Grx1 ablation resulted in the suppression of ethanol-induced NF-κB signaling, its downstream signal, and Akt signaling cascades, which are required for protection against Fas-mediated apoptosis. Accordingly, blocking NK-κB prevented Fas-induced apoptosis in WT mice but not Grx1-/- mice. Furthermore, the number of Kupffer cells and related proinflammatory cytokines, including Akt, were lower in Grx1-/- livers than those of the controls.</AbstractText><AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">Grx1 is essential for adaptation to alcohol exposure-induced oxidative injury by modulating Fas-SSG and Fas-induced apoptosis.</AbstractText><CopyrightInformation>Copyright © 2020. Published by Elsevier Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Xiaomin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Department of Ultrasound, Children's Hospital of Chongqing Medical University, Chongqing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ye</LastName><ForeName>Cuilian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; School of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Qin</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Jingyu</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Department of Ultrasound, Children's Hospital of Chongqing Medical University, Chongqing, China. Electronic address: chenjingyu@hospital.cqmu.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Chunbao</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Laboratory of Surgery, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China. Electronic address: guochunbao@hospital.cqmu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>10</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Life Sci</MedlineTA><NlmUniqueID>0375521</NlmUniqueID><ISSNLinking>0024-3205</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Ethanol</Keyword><Keyword MajorTopicYN="N">Fas</Keyword><Keyword MajorTopicYN="N">Glutaredoxin-1</Keyword><Keyword MajorTopicYN="N">Oxidant</Keyword><Keyword MajorTopicYN="N">Protein s-glutathionylation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>08</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>10</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>10</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>11</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>10</Month><Day>31</Day><Hour>5</Hour><Minute>28</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33127518</ArticleId><ArticleId IdType="pii">S0024-3205(20)31431-4</ArticleId><ArticleId IdType="doi">10.1016/j.lfs.2020.118678</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="Sun, Xiaomin" sort="Sun, Xiaomin" uniqKey="Sun X" first="Xiaomin" last="Sun">Xiaomin Sun</name></noRegion><name sortKey="Chen, Jingyu" sort="Chen, Jingyu" uniqKey="Chen J" first="Jingyu" last="Chen">Jingyu Chen</name><name sortKey="Deng, Qin" sort="Deng, Qin" uniqKey="Deng Q" first="Qin" last="Deng">Qin Deng</name><name sortKey="Guo, Chunbao" sort="Guo, Chunbao" uniqKey="Guo C" first="Chunbao" last="Guo">Chunbao Guo</name><name sortKey="Ye, Cuilian" sort="Ye, Cuilian" uniqKey="Ye C" first="Cuilian" last="Ye">Cuilian Ye</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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