Glutaredoxin 2a overexpression in macrophages promotes mitochondrial dysfunction but has little or no effect on atherogenesis in LDL-receptor null mice.
Identifieur interne : 000550 ( Main/Exploration ); précédent : 000549; suivant : 000551Glutaredoxin 2a overexpression in macrophages promotes mitochondrial dysfunction but has little or no effect on atherogenesis in LDL-receptor null mice.
Auteurs : D A Zamora [États-Unis] ; K P Downs [États-Unis] ; S L Ullevig [États-Unis] ; S. Tavakoli [États-Unis] ; H S Kim [États-Unis] ; M. Qiao [États-Unis] ; D R Greaves [Royaume-Uni] ; R. Asmis [États-Unis]Source :
- Atherosclerosis [ 1879-1484 ] ; 2015.
Descripteurs français
- KwdFr :
- Adénosine triphosphate (métabolisme), Animaux (MeSH), Aorte (anatomopathologie), Aorte (enzymologie), Apoptose (MeSH), Athérosclérose (anatomopathologie), Athérosclérose (enzymologie), Athérosclérose (génétique), Cellules cultivées (MeSH), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Indice de gravité de la maladie (MeSH), Macrophages péritonéaux (anatomopathologie), Macrophages péritonéaux (enzymologie), Maladies de l'aorte (anatomopathologie), Maladies de l'aorte (enzymologie), Maladies de l'aorte (génétique), Mitochondries (anatomopathologie), Mitochondries (enzymologie), Modèles animaux de maladie humaine (MeSH), Métabolisme énergétique (MeSH), Plaque d'athérosclérose (MeSH), Récepteurs aux lipoprotéines LDL (déficit), Récepteurs aux lipoprotéines LDL (génétique), Souris de lignée C57BL (MeSH), Souris knockout (MeSH).
- MESH :
- anatomopathologie : Aorte, Athérosclérose, Macrophages péritonéaux, Maladies de l'aorte, Mitochondries.
- déficit : Récepteurs aux lipoprotéines LDL.
- enzymologie : Aorte, Athérosclérose, Macrophages péritonéaux, Maladies de l'aorte, Mitochondries.
- génétique : Athérosclérose, Glutarédoxines, Maladies de l'aorte, Récepteurs aux lipoprotéines LDL.
- métabolisme : Adénosine triphosphate, Glutarédoxines.
- Animaux, Apoptose, Cellules cultivées, Indice de gravité de la maladie, Modèles animaux de maladie humaine, Métabolisme énergétique, Plaque d'athérosclérose, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Adenosine Triphosphate (metabolism), Animals (MeSH), Aorta (enzymology), Aorta (pathology), Aortic Diseases (enzymology), Aortic Diseases (genetics), Aortic Diseases (pathology), Apoptosis (MeSH), Atherosclerosis (enzymology), Atherosclerosis (genetics), Atherosclerosis (pathology), Cells, Cultured (MeSH), Disease Models, Animal (MeSH), Energy Metabolism (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Macrophages, Peritoneal (enzymology), Macrophages, Peritoneal (pathology), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Mitochondria (enzymology), Mitochondria (pathology), Plaque, Atherosclerotic (MeSH), Receptors, LDL (deficiency), Receptors, LDL (genetics), Severity of Illness Index (MeSH).
- MESH :
- chemical , deficiency : Receptors, LDL.
- chemical , genetics : Glutaredoxins, Receptors, LDL.
- chemical , metabolism : Adenosine Triphosphate, Glutaredoxins.
- enzymology : Aorta, Aortic Diseases, Atherosclerosis, Macrophages, Peritoneal, Mitochondria.
- genetics : Aortic Diseases, Atherosclerosis.
- pathology : Aorta, Aortic Diseases, Atherosclerosis, Macrophages, Peritoneal, Mitochondria.
- Animals, Apoptosis, Cells, Cultured, Disease Models, Animal, Energy Metabolism, Mice, Inbred C57BL, Mice, Knockout, Plaque, Atherosclerotic, Severity of Illness Index.
Abstract
AIMS
Reactive oxygen species (ROS)-mediated formation of mixed disulfides between critical cysteine residues in proteins and glutathione, a process referred to as protein S-glutathionylation, can lead to loss of enzymatic activity and protein degradation. Since mitochondria are a major source of ROS and a number of their proteins are susceptible to protein-S-glutathionylation, we examined if overexpression of mitochondrial thioltranferase glutaredoxin 2a (Grx2a) in macrophages of dyslipidemic atherosclerosis-prone mice would prevent mitochondrial dysfunction and protect against atherosclerotic lesion formation.
METHODS AND RESULTS
We generated transgenic Grx2aMac(LDLR-/-) mice, which overexpress Grx2a as an EGFP fusion protein under the control of the macrophage-specific CD68 promoter. Transgenic mice and wild type siblings were fed a high fat diet for 14 weeks at which time we assessed mitochondrial bioenergetic function in peritoneal macrophages and atherosclerotic lesion formation. Flow cytometry and Western blot analysis demonstrated transgene expression in blood monocytes and peritoneal macrophages isolated from Grx2aMac(LDLR-/-) mice, and fluorescence confocal microscopy studies confirmed that Grx2a expression was restricted to the mitochondria of monocytic cells. Live-cell bioenergetic measurements revealed impaired mitochondrial ATP turnover in macrophages isolated from Grx2aMac(LDLR-/-) mice compared to macrophages isolated from non-transgenic mice. However, despite impaired mitochondrial function in macrophages of Grx2aMac(LDLR-/-) mice, we observed no significant difference in the severity of atherosclerosis between wildtype and Grx2aMac(LDLR-/-) mice.
CONCLUSION
Our findings suggest that increasing Grx2a activity in macrophage mitochondria disrupts mitochondrial respiration and ATP production, but without affecting the proatherogenic potential of macrophages. Our data suggest that macrophages are resistant against moderate mitochondrial dysfunction and rely on alternative pathways for ATP synthesis to support the energetic requirements.
DOI: 10.1016/j.atherosclerosis.2015.04.805
PubMed: 25966442
PubMed Central: PMC4466159
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Tavakoli</name><affiliation wicri:level="1"><nlm:affiliation>Department of Radiology, University of Texas Health Science Center at San Antonio, San Antonio, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Radiology, University of Texas Health Science Center at San Antonio, San Antonio</wicri:regionArea><wicri:noRegion>San Antonio</wicri:noRegion></affiliation></author><author><name sortKey="Kim, H S" sort="Kim, H S" uniqKey="Kim H" first="H S" last="Kim">H S Kim</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio</wicri:regionArea><wicri:noRegion>University of Texas Health Science Center at San Antonio</wicri:noRegion></affiliation></author><author><name sortKey="Qiao, M" sort="Qiao, M" uniqKey="Qiao M" first="M" last="Qiao">M. Qiao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio</wicri:regionArea><wicri:noRegion>University of Texas Health Science Center at San Antonio</wicri:noRegion></affiliation></author><author><name sortKey="Greaves, D R" sort="Greaves, D R" uniqKey="Greaves D" first="D R" last="Greaves">D R Greaves</name><affiliation wicri:level="4"><nlm:affiliation>Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sir William Dunn School of Pathology, University of Oxford, Oxford</wicri:regionArea><placeName><settlement type="city">Oxford</settlement><region type="country">Angleterre</region><region type="comté" nuts="2">Oxfordshire</region></placeName><orgName type="university">Université d'Oxford</orgName></affiliation></author><author><name sortKey="Asmis, R" sort="Asmis, R" uniqKey="Asmis R" first="R" last="Asmis">R. Asmis</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio, USA; Department of Radiology, University of Texas Health Science Center at San Antonio, San Antonio, USA; Department of Biochemistry, University of Texas Health Science Center at San Antonio, USA. Electronic address: asmis@uthscsa.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio, USA; Department of Radiology, University of Texas Health Science Center at San Antonio, San Antonio, USA; Department of Biochemistry, University of Texas Health Science Center at San Antonio</wicri:regionArea><wicri:noRegion>University of Texas Health Science Center at San Antonio</wicri:noRegion></affiliation></author></analytic><series><title level="j">Atherosclerosis</title><idno type="eISSN">1879-1484</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine Triphosphate (metabolism)</term><term>Animals (MeSH)</term><term>Aorta (enzymology)</term><term>Aorta (pathology)</term><term>Aortic Diseases (enzymology)</term><term>Aortic Diseases (genetics)</term><term>Aortic Diseases (pathology)</term><term>Apoptosis (MeSH)</term><term>Atherosclerosis (enzymology)</term><term>Atherosclerosis (genetics)</term><term>Atherosclerosis (pathology)</term><term>Cells, Cultured (MeSH)</term><term>Disease Models, Animal (MeSH)</term><term>Energy Metabolism (MeSH)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Macrophages, Peritoneal (enzymology)</term><term>Macrophages, Peritoneal (pathology)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Mitochondria (enzymology)</term><term>Mitochondria (pathology)</term><term>Plaque, Atherosclerotic (MeSH)</term><term>Receptors, LDL (deficiency)</term><term>Receptors, LDL (genetics)</term><term>Severity of Illness Index (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adénosine triphosphate (métabolisme)</term><term>Animaux (MeSH)</term><term>Aorte (anatomopathologie)</term><term>Aorte (enzymologie)</term><term>Apoptose (MeSH)</term><term>Athérosclérose (anatomopathologie)</term><term>Athérosclérose (enzymologie)</term><term>Athérosclérose (génétique)</term><term>Cellules cultivées (MeSH)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Indice de gravité de la maladie (MeSH)</term><term>Macrophages péritonéaux (anatomopathologie)</term><term>Macrophages péritonéaux (enzymologie)</term><term>Maladies de l'aorte (anatomopathologie)</term><term>Maladies de l'aorte (enzymologie)</term><term>Maladies de l'aorte (génétique)</term><term>Mitochondries (anatomopathologie)</term><term>Mitochondries (enzymologie)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Métabolisme énergétique (MeSH)</term><term>Plaque d'athérosclérose (MeSH)</term><term>Récepteurs aux lipoprotéines LDL (déficit)</term><term>Récepteurs aux lipoprotéines LDL (génétique)</term><term>Souris de lignée C57BL (MeSH)</term><term>Souris knockout (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Receptors, LDL</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term><term>Receptors, LDL</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenosine Triphosphate</term><term>Glutaredoxins</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Aorte</term><term>Athérosclérose</term><term>Macrophages péritonéaux</term><term>Maladies de l'aorte</term><term>Mitochondries</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Récepteurs aux lipoprotéines LDL</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Aorte</term><term>Athérosclérose</term><term>Macrophages péritonéaux</term><term>Maladies de l'aorte</term><term>Mitochondries</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Aorta</term><term>Aortic Diseases</term><term>Atherosclerosis</term><term>Macrophages, Peritoneal</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Aortic Diseases</term><term>Atherosclerosis</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Athérosclérose</term><term>Glutarédoxines</term><term>Maladies de l'aorte</term><term>Récepteurs aux lipoprotéines LDL</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adénosine triphosphate</term><term>Glutarédoxines</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Aorta</term><term>Aortic Diseases</term><term>Atherosclerosis</term><term>Macrophages, Peritoneal</term><term>Mitochondria</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Cells, Cultured</term><term>Disease Models, Animal</term><term>Energy Metabolism</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Plaque, Atherosclerotic</term><term>Severity of Illness Index</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Cellules cultivées</term><term>Indice de gravité de la maladie</term><term>Modèles animaux de maladie humaine</term><term>Métabolisme énergétique</term><term>Plaque d'athérosclérose</term><term>Souris de lignée C57BL</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>AIMS</b></p><p>Reactive oxygen species (ROS)-mediated formation of mixed disulfides between critical cysteine residues in proteins and glutathione, a process referred to as protein S-glutathionylation, can lead to loss of enzymatic activity and protein degradation. Since mitochondria are a major source of ROS and a number of their proteins are susceptible to protein-S-glutathionylation, we examined if overexpression of mitochondrial thioltranferase glutaredoxin 2a (Grx2a) in macrophages of dyslipidemic atherosclerosis-prone mice would prevent mitochondrial dysfunction and protect against atherosclerotic lesion formation.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS AND RESULTS</b></p><p>We generated transgenic Grx2aMac(LDLR-/-) mice, which overexpress Grx2a as an EGFP fusion protein under the control of the macrophage-specific CD68 promoter. Transgenic mice and wild type siblings were fed a high fat diet for 14 weeks at which time we assessed mitochondrial bioenergetic function in peritoneal macrophages and atherosclerotic lesion formation. Flow cytometry and Western blot analysis demonstrated transgene expression in blood monocytes and peritoneal macrophages isolated from Grx2aMac(LDLR-/-) mice, and fluorescence confocal microscopy studies confirmed that Grx2a expression was restricted to the mitochondria of monocytic cells. Live-cell bioenergetic measurements revealed impaired mitochondrial ATP turnover in macrophages isolated from Grx2aMac(LDLR-/-) mice compared to macrophages isolated from non-transgenic mice. However, despite impaired mitochondrial function in macrophages of Grx2aMac(LDLR-/-) mice, we observed no significant difference in the severity of atherosclerosis between wildtype and Grx2aMac(LDLR-/-) mice.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSION</b></p><p>Our findings suggest that increasing Grx2a activity in macrophage mitochondria disrupts mitochondrial respiration and ATP production, but without affecting the proatherogenic potential of macrophages. Our data suggest that macrophages are resistant against moderate mitochondrial dysfunction and rely on alternative pathways for ATP synthesis to support the energetic requirements.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25966442</PMID><DateCompleted><Year>2016</Year><Month>03</Month><Day>08</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-1484</ISSN><JournalIssue CitedMedium="Internet"><Volume>241</Volume><Issue>1</Issue><PubDate><Year>2015</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Atherosclerosis</Title><ISOAbbreviation>Atherosclerosis</ISOAbbreviation></Journal><ArticleTitle>Glutaredoxin 2a overexpression in macrophages promotes mitochondrial dysfunction but has little or no effect on atherogenesis in LDL-receptor null mice.</ArticleTitle><Pagination><MedlinePgn>69-78</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.atherosclerosis.2015.04.805</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0021-9150(15)01023-0</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">Reactive oxygen species (ROS)-mediated formation of mixed disulfides between critical cysteine residues in proteins and glutathione, a process referred to as protein S-glutathionylation, can lead to loss of enzymatic activity and protein degradation. Since mitochondria are a major source of ROS and a number of their proteins are susceptible to protein-S-glutathionylation, we examined if overexpression of mitochondrial thioltranferase glutaredoxin 2a (Grx2a) in macrophages of dyslipidemic atherosclerosis-prone mice would prevent mitochondrial dysfunction and protect against atherosclerotic lesion formation.</AbstractText><AbstractText Label="METHODS AND RESULTS" NlmCategory="RESULTS">We generated transgenic Grx2aMac(LDLR-/-) mice, which overexpress Grx2a as an EGFP fusion protein under the control of the macrophage-specific CD68 promoter. Transgenic mice and wild type siblings were fed a high fat diet for 14 weeks at which time we assessed mitochondrial bioenergetic function in peritoneal macrophages and atherosclerotic lesion formation. Flow cytometry and Western blot analysis demonstrated transgene expression in blood monocytes and peritoneal macrophages isolated from Grx2aMac(LDLR-/-) mice, and fluorescence confocal microscopy studies confirmed that Grx2a expression was restricted to the mitochondria of monocytic cells. Live-cell bioenergetic measurements revealed impaired mitochondrial ATP turnover in macrophages isolated from Grx2aMac(LDLR-/-) mice compared to macrophages isolated from non-transgenic mice. However, despite impaired mitochondrial function in macrophages of Grx2aMac(LDLR-/-) mice, we observed no significant difference in the severity of atherosclerosis between wildtype and Grx2aMac(LDLR-/-) mice.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Our findings suggest that increasing Grx2a activity in macrophage mitochondria disrupts mitochondrial respiration and ATP production, but without affecting the proatherogenic potential of macrophages. Our data suggest that macrophages are resistant against moderate mitochondrial dysfunction and rely on alternative pathways for ATP synthesis to support the energetic requirements.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zamora</LastName><ForeName>D A</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>Department of Biology, Trinity University, San Antonio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Downs</LastName><ForeName>K P</ForeName><Initials>KP</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ullevig</LastName><ForeName>S L</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Department of Kinesiology, Health, and Nutrition, University of Texas at San Antonio, San Antonio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tavakoli</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Texas Health Science Center at San Antonio, San Antonio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>H S</ForeName><Initials>HS</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qiao</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Greaves</LastName><ForeName>D R</ForeName><Initials>DR</Initials><AffiliationInfo><Affiliation>Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Asmis</LastName><ForeName>R</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, University of Texas Health Science Center at San Antonio, USA; Department of Radiology, University of Texas Health Science Center at San Antonio, San Antonio, USA; Department of Biochemistry, University of Texas Health Science Center at San Antonio, USA. Electronic address: asmis@uthscsa.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HL115858</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>RG/10/15/28578</GrantID><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>HL70963</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 HL007446</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL115858</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL070963</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal 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