Segment-specific overexpression of redoxins after renal ischemia and reperfusion: protective roles of glutaredoxin 2, peroxiredoxin 3, and peroxiredoxin 6.
Identifieur interne : 000917 ( Main/Exploration ); précédent : 000916; suivant : 000918Segment-specific overexpression of redoxins after renal ischemia and reperfusion: protective roles of glutaredoxin 2, peroxiredoxin 3, and peroxiredoxin 6.
Auteurs : José R. Godoy [Allemagne] ; Sabrina Oesteritz ; Eva-Maria Hanschmann ; Wymke Ockenga ; Waltraud Ackermann ; Christopher Horst LilligSource :
- Free radical biology & medicine [ 1873-4596 ] ; 2011.
Descripteurs français
- KwdFr :
- Amorces ADN (MeSH), Animaux (MeSH), Glutarédoxines (physiologie), Lésion d'ischémie-reperfusion (enzymologie), Lésion d'ischémie-reperfusion (prévention et contrôle), Mâle (MeSH), Peroxiredoxin VI (physiologie), Peroxirédoxines (physiologie), Rein (vascularisation), Souris (MeSH), Souris de lignée C57BL (MeSH), Séquence nucléotidique (MeSH), Technique de Western (MeSH).
- MESH :
- enzymologie : Lésion d'ischémie-reperfusion.
- physiologie : Glutarédoxines, Peroxiredoxin VI, Peroxirédoxines.
- prévention et contrôle : Lésion d'ischémie-reperfusion.
- vascularisation : Rein.
- Amorces ADN, Animaux, Mâle, Souris, Souris de lignée C57BL, Séquence nucléotidique, Technique de Western.
English descriptors
- KwdEn :
- Animals (MeSH), Base Sequence (MeSH), Blotting, Western (MeSH), DNA Primers (MeSH), Glutaredoxins (physiology), Kidney (blood supply), Male (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Peroxiredoxin VI (physiology), Peroxiredoxins (physiology), Reperfusion Injury (enzymology), Reperfusion Injury (prevention & control).
- MESH :
- chemical , physiology : Glutaredoxins, Peroxiredoxin VI, Peroxiredoxins.
- chemical : DNA Primers.
- blood supply : Kidney.
- enzymology : Reperfusion Injury.
- prevention & control : Reperfusion Injury.
- Animals, Base Sequence, Blotting, Western, Male, Mice, Mice, Inbred C57BL.
Abstract
The disruption of redox control, i.e., oxidative stress, is one of the most destructive causes of ischemia-reperfusion (IR) injury. Thioredoxin (Trx) family proteins play a major role in the cellular response to oxidative stress. Here, we systematically investigated the levels and tissue distribution of 15 members of this family (Trx and TrxR 1 and 2, Nrx, Prx 1-6, and Grx 1-3 and 5) in mouse kidneys after induction of IR by comparing control, clamped, and contralateral organs. After IR, levels of various redoxins were quantified. Immunohistochemical analysis revealed segment-specific alterations induced by the ischemic insult. Grx2, Prx3, and Prx6 were highly expressed in proximal tubule cells. Overexpression of these proteins in HEK293 and HeLa cells subjected to hypoxia and reoxygenation revealed higher survival and proliferation rates and lower oxidative damage compared to controls. Furthermore, we report for the first time the accumulation of Grx1 at the apical side of distal convoluted cells and the specific secretion of Grx1 into the urine after IR. The differences in both the basal equipment and the segment-specific responses of the antioxidant proteins may contribute to the distinct susceptibilities and regeneration processes of the various segments of the nephron to the IR insult.
DOI: 10.1016/j.freeradbiomed.2011.04.036
PubMed: 21586322
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Godoy</name><affiliation wicri:level="3"><nlm:affiliation>Institut für Klinische Zytobiologie und Zytopathologie, Fachbereich Medizin, Philipps-Universität, DE-35037 Marburg, Germany. godoyber@staff.uni-marburg.de</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institut für Klinische Zytobiologie und Zytopathologie, Fachbereich Medizin, Philipps-Universität, DE-35037 Marburg</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Giessen</region><settlement type="city">Marbourg</settlement></placeName></affiliation></author><author><name sortKey="Oesteritz, Sabrina" sort="Oesteritz, Sabrina" uniqKey="Oesteritz S" first="Sabrina" last="Oesteritz">Sabrina Oesteritz</name></author><author><name sortKey="Hanschmann, Eva Maria" sort="Hanschmann, Eva Maria" uniqKey="Hanschmann E" first="Eva-Maria" last="Hanschmann">Eva-Maria Hanschmann</name></author><author><name sortKey="Ockenga, Wymke" sort="Ockenga, Wymke" uniqKey="Ockenga W" first="Wymke" last="Ockenga">Wymke Ockenga</name></author><author><name sortKey="Ackermann, Waltraud" sort="Ackermann, Waltraud" uniqKey="Ackermann W" first="Waltraud" last="Ackermann">Waltraud Ackermann</name></author><author><name sortKey="Lillig, Christopher Horst" sort="Lillig, Christopher Horst" uniqKey="Lillig C" first="Christopher Horst" last="Lillig">Christopher Horst Lillig</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="RBID">pubmed:21586322</idno><idno type="pmid">21586322</idno><idno type="doi">10.1016/j.freeradbiomed.2011.04.036</idno><idno type="wicri:Area/Main/Corpus">000921</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000921</idno><idno type="wicri:Area/Main/Curation">000921</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000921</idno><idno type="wicri:Area/Main/Exploration">000921</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Segment-specific overexpression of redoxins after renal ischemia and reperfusion: protective roles of glutaredoxin 2, peroxiredoxin 3, and peroxiredoxin 6.</title><author><name sortKey="Godoy, Jose R" sort="Godoy, Jose R" uniqKey="Godoy J" first="José R" last="Godoy">José R. Godoy</name><affiliation wicri:level="3"><nlm:affiliation>Institut für Klinische Zytobiologie und Zytopathologie, Fachbereich Medizin, Philipps-Universität, DE-35037 Marburg, Germany. godoyber@staff.uni-marburg.de</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institut für Klinische Zytobiologie und Zytopathologie, Fachbereich Medizin, Philipps-Universität, DE-35037 Marburg</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Giessen</region><settlement type="city">Marbourg</settlement></placeName></affiliation></author><author><name sortKey="Oesteritz, Sabrina" sort="Oesteritz, Sabrina" uniqKey="Oesteritz S" first="Sabrina" last="Oesteritz">Sabrina Oesteritz</name></author><author><name sortKey="Hanschmann, Eva Maria" sort="Hanschmann, Eva Maria" uniqKey="Hanschmann E" first="Eva-Maria" last="Hanschmann">Eva-Maria Hanschmann</name></author><author><name sortKey="Ockenga, Wymke" sort="Ockenga, Wymke" uniqKey="Ockenga W" first="Wymke" last="Ockenga">Wymke Ockenga</name></author><author><name sortKey="Ackermann, Waltraud" sort="Ackermann, Waltraud" uniqKey="Ackermann W" first="Waltraud" last="Ackermann">Waltraud Ackermann</name></author><author><name sortKey="Lillig, Christopher Horst" sort="Lillig, Christopher Horst" uniqKey="Lillig C" first="Christopher Horst" last="Lillig">Christopher Horst Lillig</name></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Base Sequence (MeSH)</term><term>Blotting, Western (MeSH)</term><term>DNA Primers (MeSH)</term><term>Glutaredoxins (physiology)</term><term>Kidney (blood supply)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Peroxiredoxin VI (physiology)</term><term>Peroxiredoxins (physiology)</term><term>Reperfusion Injury (enzymology)</term><term>Reperfusion Injury (prevention & control)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Amorces ADN (MeSH)</term><term>Animaux (MeSH)</term><term>Glutarédoxines (physiologie)</term><term>Lésion d'ischémie-reperfusion (enzymologie)</term><term>Lésion d'ischémie-reperfusion (prévention et contrôle)</term><term>Mâle (MeSH)</term><term>Peroxiredoxin VI (physiologie)</term><term>Peroxirédoxines (physiologie)</term><term>Rein (vascularisation)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Séquence nucléotidique (MeSH)</term><term>Technique de Western (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Glutaredoxins</term><term>Peroxiredoxin VI</term><term>Peroxiredoxins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>DNA Primers</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Lésion d'ischémie-reperfusion</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Reperfusion Injury</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Glutarédoxines</term><term>Peroxiredoxin VI</term><term>Peroxirédoxines</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Reperfusion Injury</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Lésion d'ischémie-reperfusion</term></keywords><keywords scheme="MESH" qualifier="vascularisation" xml:lang="fr"><term>Rein</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>Blotting, Western</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Amorces ADN</term><term>Animaux</term><term>Mâle</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Séquence nucléotidique</term><term>Technique de Western</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The disruption of redox control, i.e., oxidative stress, is one of the most destructive causes of ischemia-reperfusion (IR) injury. Thioredoxin (Trx) family proteins play a major role in the cellular response to oxidative stress. Here, we systematically investigated the levels and tissue distribution of 15 members of this family (Trx and TrxR 1 and 2, Nrx, Prx 1-6, and Grx 1-3 and 5) in mouse kidneys after induction of IR by comparing control, clamped, and contralateral organs. After IR, levels of various redoxins were quantified. Immunohistochemical analysis revealed segment-specific alterations induced by the ischemic insult. Grx2, Prx3, and Prx6 were highly expressed in proximal tubule cells. Overexpression of these proteins in HEK293 and HeLa cells subjected to hypoxia and reoxygenation revealed higher survival and proliferation rates and lower oxidative damage compared to controls. Furthermore, we report for the first time the accumulation of Grx1 at the apical side of distal convoluted cells and the specific secretion of Grx1 into the urine after IR. The differences in both the basal equipment and the segment-specific responses of the antioxidant proteins may contribute to the distinct susceptibilities and regeneration processes of the various segments of the nephron to the IR insult.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21586322</PMID><DateCompleted><Year>2011</Year><Month>10</Month><Day>27</Day></DateCompleted><DateRevised><Year>2011</Year><Month>06</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN><JournalIssue CitedMedium="Internet"><Volume>51</Volume><Issue>2</Issue><PubDate><Year>2011</Year><Month>Jul</Month><Day>15</Day></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation></Journal><ArticleTitle>Segment-specific overexpression of redoxins after renal ischemia and reperfusion: protective roles of glutaredoxin 2, peroxiredoxin 3, and peroxiredoxin 6.</ArticleTitle><Pagination><MedlinePgn>552-61</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2011.04.036</ELocationID><Abstract><AbstractText>The disruption of redox control, i.e., oxidative stress, is one of the most destructive causes of ischemia-reperfusion (IR) injury. Thioredoxin (Trx) family proteins play a major role in the cellular response to oxidative stress. Here, we systematically investigated the levels and tissue distribution of 15 members of this family (Trx and TrxR 1 and 2, Nrx, Prx 1-6, and Grx 1-3 and 5) in mouse kidneys after induction of IR by comparing control, clamped, and contralateral organs. After IR, levels of various redoxins were quantified. Immunohistochemical analysis revealed segment-specific alterations induced by the ischemic insult. Grx2, Prx3, and Prx6 were highly expressed in proximal tubule cells. Overexpression of these proteins in HEK293 and HeLa cells subjected to hypoxia and reoxygenation revealed higher survival and proliferation rates and lower oxidative damage compared to controls. Furthermore, we report for the first time the accumulation of Grx1 at the apical side of distal convoluted cells and the specific secretion of Grx1 into the urine after IR. The differences in both the basal equipment and the segment-specific responses of the antioxidant proteins may contribute to the distinct susceptibilities and regeneration processes of the various segments of the nephron to the IR insult.</AbstractText><CopyrightInformation>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Godoy</LastName><ForeName>José R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Institut für Klinische Zytobiologie und Zytopathologie, Fachbereich Medizin, Philipps-Universität, DE-35037 Marburg, Germany. godoyber@staff.uni-marburg.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oesteritz</LastName><ForeName>Sabrina</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Hanschmann</LastName><ForeName>Eva-Maria</ForeName><Initials>EM</Initials></Author><Author ValidYN="Y"><LastName>Ockenga</LastName><ForeName>Wymke</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Ackermann</LastName><ForeName>Waltraud</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Lillig</LastName><ForeName>Christopher Horst</ForeName><Initials>CH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>04</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Free Radic Biol Med</MedlineTA><NlmUniqueID>8709159</NlmUniqueID><ISSNLinking>0891-5849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017931">DNA Primers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.15</RegistryNumber><NameOfSubstance UI="D054465">Peroxiredoxin VI</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.15</RegistryNumber><NameOfSubstance UI="D054464">Peroxiredoxins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017931" MajorTopicYN="N">DNA Primers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007668" MajorTopicYN="N">Kidney</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="Y">blood supply</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054465" MajorTopicYN="N">Peroxiredoxin VI</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054464" MajorTopicYN="N">Peroxiredoxins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015427" MajorTopicYN="N">Reperfusion Injury</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>02</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2011</Year><Month>04</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>04</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>5</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>5</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">21586322</ArticleId><ArticleId IdType="pii">S0891-5849(11)00277-2</ArticleId><ArticleId IdType="doi">10.1016/j.freeradbiomed.2011.04.036</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>District de Giessen</li><li>Hesse (Land)</li></region><settlement><li>Marbourg</li></settlement></list><tree><noCountry><name sortKey="Ackermann, Waltraud" sort="Ackermann, Waltraud" uniqKey="Ackermann W" first="Waltraud" last="Ackermann">Waltraud Ackermann</name><name sortKey="Hanschmann, Eva Maria" sort="Hanschmann, Eva Maria" uniqKey="Hanschmann E" first="Eva-Maria" last="Hanschmann">Eva-Maria Hanschmann</name><name sortKey="Lillig, Christopher Horst" sort="Lillig, Christopher Horst" uniqKey="Lillig C" first="Christopher Horst" last="Lillig">Christopher Horst Lillig</name><name sortKey="Ockenga, Wymke" sort="Ockenga, Wymke" uniqKey="Ockenga W" first="Wymke" last="Ockenga">Wymke Ockenga</name><name sortKey="Oesteritz, Sabrina" sort="Oesteritz, Sabrina" uniqKey="Oesteritz S" first="Sabrina" last="Oesteritz">Sabrina Oesteritz</name></noCountry><country name="Allemagne"><region name="Hesse (Land)"><name sortKey="Godoy, Jose R" sort="Godoy, Jose R" uniqKey="Godoy J" first="José R" last="Godoy">José R. 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