Glutaredoxin-2 and Sirtuin-3 deficiencies impair cardiac mitochondrial energetics but their effects are not additive.
Identifieur interne : 000066 ( Main/Exploration ); précédent : 000065; suivant : 000067Glutaredoxin-2 and Sirtuin-3 deficiencies impair cardiac mitochondrial energetics but their effects are not additive.
Auteurs : Neoma T. Boardman [Norvège] ; Baher Migally [Canada] ; Chantal Pileggi [Canada] ; Gaganvir S. Parmar [Canada] ; Jian Ying Xuan [Canada] ; Keir Menzies [Canada] ; Mary-Ellen Harper [Canada]Source :
- Biochimica et biophysica acta. Molecular basis of disease [ 1879-260X ] ; 2020.
Abstract
Altered redox biology and oxidative stress have been implicated in the progression of heart failure. Glutaredoxin-2 (GRX2) is a glutathione-dependent oxidoreductase and catalyzes the reversible deglutathionylation of mitochondrial proteins. Sirtuin-3 (SIRT3) is a class III histone deacetylase and regulates lysine acetylation in mitochondria. Both GRX2 and SIRT3 are considered as key in the protection against oxidative damage in the myocardium. Knockout of either contributes to adverse heart pathologies including hypertrophy, hypertension, and cardiac dysfunction. Here, we created and characterized a GRX2 and SIRT3 double-knockout mouse model, hypothesizing that their deletions would have an additive effect on oxidative stress, and exacerbate mitochondrial function and myocardial structural remodeling. Wildtype, single-gene knockout (Sirt3-/-, Grx2-/-), and double-knockout mice (Grx2-/-/Sirt3-/-) were compared in heart weight, histology, mitochondrial respiration and H2O2 production. Overall, the hearts from Grx2-/-/Sirt3-/- mice displayed increased fibrosis and hypertrophy versus wildtype. In the Grx2-/- and the Sirt3-/- we observed changes in mitochondrial oxidative capacity, however this was associated with elevated H2O2 emission only in the Sirt3-/-. Similar changes were observed but not worsened in hearts from Grx2-/-/Sirt3-/- mice, suggesting that these changes were not additive. In human myocardium, using genetic and histopathological data from the human Genotype-Tissue Expression consortium, we confirmed that SIRT3 expression correlates inversely with heart pathology. Altogether, GRX2 and SIRT3 are important in the control of cardiac mitochondrial redox and oxidative processes, but their combined absence does not exacerbate effects, consistent with the overall conclusion that they function together in the complex redox and antioxidant systems in the heart.
DOI: 10.1016/j.bbadis.2020.165982
PubMed: 33002579
Affiliations:
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Boardman</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada; Department of Medical Biology, Faculty of Health Sciences, UiT-Arctic University of Norway, Tromsø, Norway.</nlm:affiliation><country xml:lang="fr">Norvège</country><wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada; Department of Medical Biology, Faculty of Health Sciences, UiT-Arctic University of Norway, Tromsø</wicri:regionArea><wicri:noRegion>Tromsø</wicri:noRegion></affiliation></author><author><name sortKey="Migally, Baher" sort="Migally, Baher" uniqKey="Migally B" first="Baher" last="Migally">Baher Migally</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Pileggi, Chantal" sort="Pileggi, Chantal" uniqKey="Pileggi C" first="Chantal" last="Pileggi">Chantal Pileggi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Parmar, Gaganvir S" sort="Parmar, Gaganvir S" uniqKey="Parmar G" first="Gaganvir S" last="Parmar">Gaganvir S. Parmar</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Xuan, Jian Ying" sort="Xuan, Jian Ying" uniqKey="Xuan J" first="Jian Ying" last="Xuan">Jian Ying Xuan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Menzies, Keir" sort="Menzies, Keir" uniqKey="Menzies K" first="Keir" last="Menzies">Keir Menzies</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada; Interdisciplinary School of Health Sciences, Faculty of Health Sciences, University of Ottawa, Ottawa, ON, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada; Interdisciplinary School of Health Sciences, Faculty of Health Sciences, University of Ottawa, Ottawa, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Harper, Mary Ellen" sort="Harper, Mary Ellen" uniqKey="Harper M" first="Mary-Ellen" last="Harper">Mary-Ellen Harper</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. Electronic address: mharper@uottawa.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochimica et biophysica acta. Molecular basis of disease</title><idno type="eISSN">1879-260X</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">Altered redox biology and oxidative stress have been implicated in the progression of heart failure. Glutaredoxin-2 (GRX2) is a glutathione-dependent oxidoreductase and catalyzes the reversible deglutathionylation of mitochondrial proteins. Sirtuin-3 (SIRT3) is a class III histone deacetylase and regulates lysine acetylation in mitochondria. Both GRX2 and SIRT3 are considered as key in the protection against oxidative damage in the myocardium. Knockout of either contributes to adverse heart pathologies including hypertrophy, hypertension, and cardiac dysfunction. Here, we created and characterized a GRX2 and SIRT3 double-knockout mouse model, hypothesizing that their deletions would have an additive effect on oxidative stress, and exacerbate mitochondrial function and myocardial structural remodeling. Wildtype, single-gene knockout (Sirt3<sup>-/-</sup>, Grx2<sup>-/-</sup>), and double-knockout mice (Grx2<sup>-/-</sup>/Sirt3<sup>-/-</sup>) were compared in heart weight, histology, mitochondrial respiration and H<sub>2</sub>O<sub>2</sub> production. Overall, the hearts from Grx2<sup>-/-</sup>/Sirt3<sup>-/-</sup> mice displayed increased fibrosis and hypertrophy versus wildtype. In the Grx2<sup>-/-</sup> and the Sirt3<sup>-/-</sup> we observed changes in mitochondrial oxidative capacity, however this was associated with elevated H<sub>2</sub>O<sub>2</sub> emission only in the Sirt3<sup>-/-</sup>. Similar changes were observed but not worsened in hearts from Grx2<sup>-/-</sup>/Sirt3<sup>-/-</sup> mice, suggesting that these changes were not additive. In human myocardium, using genetic and histopathological data from the human Genotype-Tissue Expression consortium, we confirmed that SIRT3 expression correlates inversely with heart pathology. Altogether, GRX2 and SIRT3 are important in the control of cardiac mitochondrial redox and oxidative processes, but their combined absence does not exacerbate effects, consistent with the overall conclusion that they function together in the complex redox and antioxidant systems in the heart.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">33002579</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-260X</ISSN><JournalIssue CitedMedium="Internet"><Volume>1867</Volume><Issue>1</Issue><PubDate><Year>2020</Year><Month>Sep</Month><Day>28</Day></PubDate></JournalIssue><Title>Biochimica et biophysica acta. Molecular basis of disease</Title><ISOAbbreviation>Biochim Biophys Acta Mol Basis Dis</ISOAbbreviation></Journal><ArticleTitle>Glutaredoxin-2 and Sirtuin-3 deficiencies impair cardiac mitochondrial energetics but their effects are not additive.</ArticleTitle><Pagination><MedlinePgn>165982</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0925-4439(20)30330-6</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbadis.2020.165982</ELocationID><Abstract><AbstractText>Altered redox biology and oxidative stress have been implicated in the progression of heart failure. Glutaredoxin-2 (GRX2) is a glutathione-dependent oxidoreductase and catalyzes the reversible deglutathionylation of mitochondrial proteins. Sirtuin-3 (SIRT3) is a class III histone deacetylase and regulates lysine acetylation in mitochondria. Both GRX2 and SIRT3 are considered as key in the protection against oxidative damage in the myocardium. Knockout of either contributes to adverse heart pathologies including hypertrophy, hypertension, and cardiac dysfunction. Here, we created and characterized a GRX2 and SIRT3 double-knockout mouse model, hypothesizing that their deletions would have an additive effect on oxidative stress, and exacerbate mitochondrial function and myocardial structural remodeling. Wildtype, single-gene knockout (Sirt3<sup>-/-</sup>, Grx2<sup>-/-</sup>), and double-knockout mice (Grx2<sup>-/-</sup>/Sirt3<sup>-/-</sup>) were compared in heart weight, histology, mitochondrial respiration and H<sub>2</sub>O<sub>2</sub> production. Overall, the hearts from Grx2<sup>-/-</sup>/Sirt3<sup>-/-</sup> mice displayed increased fibrosis and hypertrophy versus wildtype. In the Grx2<sup>-/-</sup> and the Sirt3<sup>-/-</sup> we observed changes in mitochondrial oxidative capacity, however this was associated with elevated H<sub>2</sub>O<sub>2</sub> emission only in the Sirt3<sup>-/-</sup>. Similar changes were observed but not worsened in hearts from Grx2<sup>-/-</sup>/Sirt3<sup>-/-</sup> mice, suggesting that these changes were not additive. In human myocardium, using genetic and histopathological data from the human Genotype-Tissue Expression consortium, we confirmed that SIRT3 expression correlates inversely with heart pathology. Altogether, GRX2 and SIRT3 are important in the control of cardiac mitochondrial redox and oxidative processes, but their combined absence does not exacerbate effects, consistent with the overall conclusion that they function together in the complex redox and antioxidant systems in the heart.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Boardman</LastName><ForeName>Neoma T</ForeName><Initials>NT</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada; Department of Medical Biology, Faculty of Health Sciences, UiT-Arctic University of Norway, Tromsø, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Migally</LastName><ForeName>Baher</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pileggi</LastName><ForeName>Chantal</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parmar</LastName><ForeName>Gaganvir S</ForeName><Initials>GS</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xuan</LastName><ForeName>Jian Ying</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Menzies</LastName><ForeName>Keir</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada; Interdisciplinary School of Health Sciences, Faculty of Health Sciences, University of Ottawa, Ottawa, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harper</LastName><ForeName>Mary-Ellen</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Ottawa Institute of Systems Biology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. Electronic address: mharper@uottawa.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>09</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochim Biophys Acta Mol Basis Dis</MedlineTA><NlmUniqueID>101731730</NlmUniqueID><ISSNLinking>0925-4439</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Fibrosis</Keyword><Keyword MajorTopicYN="N">Glutathione</Keyword><Keyword MajorTopicYN="N">Hypertrophy</Keyword><Keyword MajorTopicYN="N">Mitochondria</Keyword><Keyword MajorTopicYN="N">Oxidative phosphorylation</Keyword><Keyword MajorTopicYN="N">Oxidative stress</Keyword><Keyword MajorTopicYN="N">Reactive oxygen species</Keyword><Keyword MajorTopicYN="N">Redox</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>05</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>09</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>09</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>10</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>10</Month><Day>1</Day><Hour>20</Hour><Minute>11</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33002579</ArticleId><ArticleId IdType="pii">S0925-4439(20)30330-6</ArticleId><ArticleId IdType="doi">10.1016/j.bbadis.2020.165982</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li><li>Norvège</li></country></list><tree><country name="Norvège"><noRegion><name sortKey="Boardman, Neoma T" sort="Boardman, Neoma T" uniqKey="Boardman N" first="Neoma T" last="Boardman">Neoma T. Boardman</name></noRegion></country><country name="Canada"><noRegion><name sortKey="Migally, Baher" sort="Migally, Baher" uniqKey="Migally B" first="Baher" last="Migally">Baher Migally</name></noRegion><name sortKey="Harper, Mary Ellen" sort="Harper, Mary Ellen" uniqKey="Harper M" first="Mary-Ellen" last="Harper">Mary-Ellen Harper</name><name sortKey="Menzies, Keir" sort="Menzies, Keir" uniqKey="Menzies K" first="Keir" last="Menzies">Keir Menzies</name><name sortKey="Parmar, Gaganvir S" sort="Parmar, Gaganvir S" uniqKey="Parmar G" first="Gaganvir S" last="Parmar">Gaganvir S. Parmar</name><name sortKey="Pileggi, Chantal" sort="Pileggi, Chantal" uniqKey="Pileggi C" first="Chantal" last="Pileggi">Chantal Pileggi</name><name sortKey="Xuan, Jian Ying" sort="Xuan, Jian Ying" uniqKey="Xuan J" first="Jian Ying" last="Xuan">Jian Ying Xuan</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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