Frataxin deficiency leads to defects in expression of antioxidants and Nrf2 expression in dorsal root ganglia of the Friedreich's ataxia YG8R mouse model.
Identifieur interne : 000766 ( Main/Exploration ); précédent : 000765; suivant : 000767Frataxin deficiency leads to defects in expression of antioxidants and Nrf2 expression in dorsal root ganglia of the Friedreich's ataxia YG8R mouse model.
Auteurs : Yuxi Shan [États-Unis] ; Robert A. Schoenfeld ; Genki Hayashi ; Eleonora Napoli ; Tasuku Akiyama ; Mirela Iodi Carstens ; Earl E. Carstens ; Mark A. Pook ; Gino A. CortopassiSource :
- Antioxidants & redox signaling [ 1557-7716 ] ; 2013.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Antioxydants (métabolisme), Ataxie de Friedreich (génétique), Ataxie de Friedreich (métabolisme), Cellules HeLa (MeSH), Cellules cultivées (MeSH), Facteur-2 apparenté à NF-E2 (biosynthèse), Facteur-2 apparenté à NF-E2 (génétique), Ganglions sensitifs des nerfs spinaux (métabolisme), Humains (MeSH), Modèles animaux de maladie humaine (MeSH), Protéines de liaison au fer (génétique), Protéines de liaison au fer (métabolisme), Rats (MeSH), Souris (MeSH), Souris de lignée C57BL (MeSH).
- MESH :
- biosynthèse : Facteur-2 apparenté à NF-E2.
- génétique : Ataxie de Friedreich, Facteur-2 apparenté à NF-E2, Protéines de liaison au fer.
- métabolisme : Antioxydants, Ataxie de Friedreich, Ganglions sensitifs des nerfs spinaux, Protéines de liaison au fer.
- Animaux, Cellules HeLa, Cellules cultivées, Humains, Modèles animaux de maladie humaine, Rats, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Animals (MeSH), Antioxidants (metabolism), Cells, Cultured (MeSH), Disease Models, Animal (MeSH), Friedreich Ataxia (genetics), Friedreich Ataxia (metabolism), Ganglia, Spinal (metabolism), HeLa Cells (MeSH), Humans (MeSH), Iron-Binding Proteins (genetics), Iron-Binding Proteins (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), NF-E2-Related Factor 2 (biosynthesis), NF-E2-Related Factor 2 (genetics), Rats (MeSH).
- MESH :
- chemical , biosynthesis : NF-E2-Related Factor 2.
- chemical , genetics : Iron-Binding Proteins, NF-E2-Related Factor 2.
- chemical , metabolism : Antioxidants, Iron-Binding Proteins.
- genetics : Friedreich Ataxia.
- metabolism : Friedreich Ataxia, Ganglia, Spinal.
- Animals, Cells, Cultured, Disease Models, Animal, HeLa Cells, Humans, Mice, Mice, Inbred C57BL, Rats.
Abstract
AIMS
Oxidative stress is thought to be involved in Friedreich's ataxia (FRDA), yet it has not been demonstrated in the target neurons that are first to degenerate. Using the YG8R mouse model of FRDA, microarray and neuritic growth experiments were carried out in the dorsal root ganglion (DRG), the primary site of neurodegeneration in this disease.
RESULTS
YG8R hemizygous mice exhibited defects in movement, and DRG neurites had growth defects. Microarray of DRG tissue identified decreased transcripts encoding the antioxidants, including peroxiredoxins, glutaredoxins, and glutathione S-transferase, and these were confirmed by immunoblots and quantitative real-time PCR. Because the decreased gene transcripts are the known targets of the antioxidant transcription factor nuclear factor-E2-related factor-2 (Nrf2), Nrf2 expression was measured; it was significantly decreased at the transcript and protein level in both the DRG and the cerebella of the YG8R hemizygous mouse; further, frataxin expression was significantly correlated with Nrf2 expression. Functionally, in YG8R hemizygous DRG, the total glutathione levels were reduced and explanted cells were more sensitive to the thioredoxin reductase (TxnRD) inhibitor auranofin, a thiol oxidant. In cell models of FRDA, including Schwann and the DRG, frataxin deficiency caused a decreased expression of the Nrf2 protein level in the nucleus, but not a defect in its translocation from the cytosol. Further, frataxin-deficient cells had decreased enzyme activity and expression of TxnRD, which is regulated by Nrf2, and were sensitive the TxnRD inhibitor auranofin.
INNOVATION AND CONCLUSION
These results support a mechanistic hypothesis in which frataxin deficiency decreases Nrf2 expression in vivo, causing the sensitivity to oxidative stress in target tissues the DRG and the cerebella, which contributes to the process of neurodegeneration.
DOI: 10.1089/ars.2012.4537
PubMed: 23350650
PubMed Central: PMC3797453
Affiliations:
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Schoenfeld</name></author><author><name sortKey="Hayashi, Genki" sort="Hayashi, Genki" uniqKey="Hayashi G" first="Genki" last="Hayashi">Genki Hayashi</name></author><author><name sortKey="Napoli, Eleonora" sort="Napoli, Eleonora" uniqKey="Napoli E" first="Eleonora" last="Napoli">Eleonora Napoli</name></author><author><name sortKey="Akiyama, Tasuku" sort="Akiyama, Tasuku" uniqKey="Akiyama T" first="Tasuku" last="Akiyama">Tasuku Akiyama</name></author><author><name sortKey="Iodi Carstens, Mirela" sort="Iodi Carstens, Mirela" uniqKey="Iodi Carstens M" first="Mirela" last="Iodi Carstens">Mirela Iodi Carstens</name></author><author><name sortKey="Carstens, Earl E" sort="Carstens, Earl E" uniqKey="Carstens E" first="Earl E" last="Carstens">Earl E. Carstens</name></author><author><name sortKey="Pook, Mark A" sort="Pook, Mark A" uniqKey="Pook M" first="Mark A" last="Pook">Mark A. 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Schoenfeld</name></author><author><name sortKey="Hayashi, Genki" sort="Hayashi, Genki" uniqKey="Hayashi G" first="Genki" last="Hayashi">Genki Hayashi</name></author><author><name sortKey="Napoli, Eleonora" sort="Napoli, Eleonora" uniqKey="Napoli E" first="Eleonora" last="Napoli">Eleonora Napoli</name></author><author><name sortKey="Akiyama, Tasuku" sort="Akiyama, Tasuku" uniqKey="Akiyama T" first="Tasuku" last="Akiyama">Tasuku Akiyama</name></author><author><name sortKey="Iodi Carstens, Mirela" sort="Iodi Carstens, Mirela" uniqKey="Iodi Carstens M" first="Mirela" last="Iodi Carstens">Mirela Iodi Carstens</name></author><author><name sortKey="Carstens, Earl E" sort="Carstens, Earl E" uniqKey="Carstens E" first="Earl E" last="Carstens">Earl E. Carstens</name></author><author><name sortKey="Pook, Mark A" sort="Pook, Mark A" uniqKey="Pook M" first="Mark A" last="Pook">Mark A. Pook</name></author><author><name sortKey="Cortopassi, Gino A" sort="Cortopassi, Gino A" uniqKey="Cortopassi G" first="Gino A" last="Cortopassi">Gino A. Cortopassi</name></author></analytic><series><title level="j">Antioxidants & redox signaling</title><idno type="eISSN">1557-7716</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Antioxidants (metabolism)</term><term>Cells, Cultured (MeSH)</term><term>Disease Models, Animal (MeSH)</term><term>Friedreich Ataxia (genetics)</term><term>Friedreich Ataxia (metabolism)</term><term>Ganglia, Spinal (metabolism)</term><term>HeLa Cells (MeSH)</term><term>Humans (MeSH)</term><term>Iron-Binding Proteins (genetics)</term><term>Iron-Binding Proteins (metabolism)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>NF-E2-Related Factor 2 (biosynthesis)</term><term>NF-E2-Related Factor 2 (genetics)</term><term>Rats (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Antioxydants (métabolisme)</term><term>Ataxie de Friedreich (génétique)</term><term>Ataxie de Friedreich (métabolisme)</term><term>Cellules HeLa (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Facteur-2 apparenté à NF-E2 (biosynthèse)</term><term>Facteur-2 apparenté à NF-E2 (génétique)</term><term>Ganglions sensitifs des nerfs spinaux (métabolisme)</term><term>Humains (MeSH)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Protéines de liaison au fer (génétique)</term><term>Protéines de liaison au fer (métabolisme)</term><term>Rats (MeSH)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>NF-E2-Related Factor 2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Iron-Binding Proteins</term><term>NF-E2-Related Factor 2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antioxidants</term><term>Iron-Binding Proteins</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Facteur-2 apparenté à NF-E2</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Friedreich Ataxia</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Ataxie de Friedreich</term><term>Facteur-2 apparenté à NF-E2</term><term>Protéines de liaison au fer</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Friedreich Ataxia</term><term>Ganglia, Spinal</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antioxydants</term><term>Ataxie de Friedreich</term><term>Ganglions sensitifs des nerfs spinaux</term><term>Protéines de liaison au fer</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Disease Models, Animal</term><term>HeLa Cells</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Rats</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules HeLa</term><term>Cellules cultivées</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Rats</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>AIMS</b></p><p>Oxidative stress is thought to be involved in Friedreich's ataxia (FRDA), yet it has not been demonstrated in the target neurons that are first to degenerate. Using the YG8R mouse model of FRDA, microarray and neuritic growth experiments were carried out in the dorsal root ganglion (DRG), the primary site of neurodegeneration in this disease.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>YG8R hemizygous mice exhibited defects in movement, and DRG neurites had growth defects. Microarray of DRG tissue identified decreased transcripts encoding the antioxidants, including peroxiredoxins, glutaredoxins, and glutathione S-transferase, and these were confirmed by immunoblots and quantitative real-time PCR. Because the decreased gene transcripts are the known targets of the antioxidant transcription factor nuclear factor-E2-related factor-2 (Nrf2), Nrf2 expression was measured; it was significantly decreased at the transcript and protein level in both the DRG and the cerebella of the YG8R hemizygous mouse; further, frataxin expression was significantly correlated with Nrf2 expression. Functionally, in YG8R hemizygous DRG, the total glutathione levels were reduced and explanted cells were more sensitive to the thioredoxin reductase (TxnRD) inhibitor auranofin, a thiol oxidant. In cell models of FRDA, including Schwann and the DRG, frataxin deficiency caused a decreased expression of the Nrf2 protein level in the nucleus, but not a defect in its translocation from the cytosol. Further, frataxin-deficient cells had decreased enzyme activity and expression of TxnRD, which is regulated by Nrf2, and were sensitive the TxnRD inhibitor auranofin.</p></div><div type="abstract" xml:lang="en"><p><b>INNOVATION AND CONCLUSION</b></p><p>These results support a mechanistic hypothesis in which frataxin deficiency decreases Nrf2 expression in vivo, causing the sensitivity to oxidative stress in target tissues the DRG and the cerebella, which contributes to the process of neurodegeneration.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23350650</PMID><DateCompleted><Year>2014</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-7716</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>13</Issue><PubDate><Year>2013</Year><Month>Nov</Month><Day>01</Day></PubDate></JournalIssue><Title>Antioxidants & redox signaling</Title><ISOAbbreviation>Antioxid Redox Signal</ISOAbbreviation></Journal><ArticleTitle>Frataxin deficiency leads to defects in expression of antioxidants and Nrf2 expression in dorsal root ganglia of the Friedreich's ataxia YG8R mouse model.</ArticleTitle><Pagination><MedlinePgn>1481-93</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1089/ars.2012.4537</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">Oxidative stress is thought to be involved in Friedreich's ataxia (FRDA), yet it has not been demonstrated in the target neurons that are first to degenerate. Using the YG8R mouse model of FRDA, microarray and neuritic growth experiments were carried out in the dorsal root ganglion (DRG), the primary site of neurodegeneration in this disease.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">YG8R hemizygous mice exhibited defects in movement, and DRG neurites had growth defects. Microarray of DRG tissue identified decreased transcripts encoding the antioxidants, including peroxiredoxins, glutaredoxins, and glutathione S-transferase, and these were confirmed by immunoblots and quantitative real-time PCR. Because the decreased gene transcripts are the known targets of the antioxidant transcription factor nuclear factor-E2-related factor-2 (Nrf2), Nrf2 expression was measured; it was significantly decreased at the transcript and protein level in both the DRG and the cerebella of the YG8R hemizygous mouse; further, frataxin expression was significantly correlated with Nrf2 expression. Functionally, in YG8R hemizygous DRG, the total glutathione levels were reduced and explanted cells were more sensitive to the thioredoxin reductase (TxnRD) inhibitor auranofin, a thiol oxidant. In cell models of FRDA, including Schwann and the DRG, frataxin deficiency caused a decreased expression of the Nrf2 protein level in the nucleus, but not a defect in its translocation from the cytosol. Further, frataxin-deficient cells had decreased enzyme activity and expression of TxnRD, which is regulated by Nrf2, and were sensitive the TxnRD inhibitor auranofin.</AbstractText><AbstractText Label="INNOVATION AND CONCLUSION" NlmCategory="CONCLUSIONS">These results support a mechanistic hypothesis in which frataxin deficiency decreases Nrf2 expression in vivo, causing the sensitivity to oxidative stress in target tissues the DRG and the cerebella, which contributes to the process of neurodegeneration.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shan</LastName><ForeName>Yuxi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>1 Department of Molecular Biosciences, University of California , Davis, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schoenfeld</LastName><ForeName>Robert A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Hayashi</LastName><ForeName>Genki</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Napoli</LastName><ForeName>Eleonora</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Akiyama</LastName><ForeName>Tasuku</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Iodi Carstens</LastName><ForeName>Mirela</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Carstens</LastName><ForeName>Earl E</ForeName><Initials>EE</Initials></Author><Author ValidYN="Y"><LastName>Pook</LastName><ForeName>Mark A</ForeName><Initials>MA</Initials></Author><Author ValidYN="Y"><LastName>Cortopassi</LastName><ForeName>Gino A</ForeName><Initials>GA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AG11967</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG23311</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>USPHS EY12245</GrantID><Acronym>EY</Acronym><Agency>NEI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NIA 5R01AG16719-12</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG16719</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS077777</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>03</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Antioxid Redox Signal</MedlineTA><NlmUniqueID>100888899</NlmUniqueID><ISSNLinking>1523-0864</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D033862">Iron-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495636">Nfe2l2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C098527">frataxin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName><QualifierName 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Schoenfeld</name></noCountry><country name="États-Unis"><region name="Californie"><name sortKey="Shan, Yuxi" sort="Shan, Yuxi" uniqKey="Shan Y" first="Yuxi" last="Shan">Yuxi Shan</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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