Redoxins in peripheral neurons after sciatic nerve injury.
Identifieur interne : 000510 ( Main/Exploration ); précédent : 000509; suivant : 000511Redoxins in peripheral neurons after sciatic nerve injury.
Auteurs : Lucie Valek [Allemagne] ; Maike Kanngie Er [Allemagne] ; Annett H Ussler [Allemagne] ; Nitin Agarwal [Allemagne] ; Christopher Horst Lillig [Allemagne] ; Irmgard Tegeder [Allemagne]Source :
- Free radical biology & medicine [ 1873-4596 ] ; 2015.
Descripteurs français
- KwdFr :
- ARN messager (analyse), Animaux (MeSH), Femelle (MeSH), Ganglions sensitifs des nerfs spinaux (anatomopathologie), Ganglions sensitifs des nerfs spinaux (métabolisme), Glutarédoxines (biosynthèse), Immunohistochimie (MeSH), Modèles animaux de maladie humaine (MeSH), Mâle (MeSH), Nerf ischiatique (traumatismes), Neurones (anatomopathologie), Neurones (métabolisme), Neuropathie du nerf sciatique (anatomopathologie), Neuropathie du nerf sciatique (métabolisme), Névroglie (anatomopathologie), Névroglie (métabolisme), Oxydoréduction (MeSH), Peroxirédoxines (biosynthèse), RT-PCR (MeSH), Régulation positive (MeSH), Souris (MeSH), Souris knockout (MeSH), Thiorédoxines (biosynthèse).
- MESH :
- analyse : ARN messager.
- anatomopathologie : Ganglions sensitifs des nerfs spinaux, Neurones, Neuropathie du nerf sciatique, Névroglie.
- biosynthèse : Glutarédoxines, Peroxirédoxines, Thiorédoxines.
- métabolisme : Ganglions sensitifs des nerfs spinaux, Neurones, Neuropathie du nerf sciatique, Névroglie.
- traumatismes : Nerf ischiatique.
- Animaux, Femelle, Immunohistochimie, Modèles animaux de maladie humaine, Mâle, Oxydoréduction, RT-PCR, Régulation positive, Souris, Souris knockout.
English descriptors
- KwdEn :
- Animals (MeSH), Disease Models, Animal (MeSH), Female (MeSH), Ganglia, Spinal (metabolism), Ganglia, Spinal (pathology), Glutaredoxins (biosynthesis), Immunohistochemistry (MeSH), Male (MeSH), Mice (MeSH), Mice, Knockout (MeSH), Neuroglia (metabolism), Neuroglia (pathology), Neurons (metabolism), Neurons (pathology), Oxidation-Reduction (MeSH), Peroxiredoxins (biosynthesis), RNA, Messenger (analysis), Reverse Transcriptase Polymerase Chain Reaction (MeSH), Sciatic Nerve (injuries), Sciatic Neuropathy (metabolism), Sciatic Neuropathy (pathology), Thioredoxins (biosynthesis), Up-Regulation (MeSH).
- MESH :
- chemical , analysis : RNA, Messenger.
- chemical , biosynthesis : Glutaredoxins, Peroxiredoxins, Thioredoxins.
- injuries : Sciatic Nerve.
- metabolism : Ganglia, Spinal, Neuroglia, Neurons, Sciatic Neuropathy.
- pathology : Ganglia, Spinal, Neuroglia, Neurons, Sciatic Neuropathy.
- Animals, Disease Models, Animal, Female, Immunohistochemistry, Male, Mice, Mice, Knockout, Oxidation-Reduction, Reverse Transcriptase Polymerase Chain Reaction, Up-Regulation.
Abstract
Peripheral nerve injury causes redox stress in injured neurons by upregulations of pro-oxidative enzymes, but most neurons survive suggesting an activation of endogenous defense against the imbalance. As potential candidates we assessed thioredoxin-fold proteins, called redoxins, which maintain redox homeostasis by reduction of hydrogen peroxide or protein dithiol-disulfide exchange. Using a histologic approach, we show that the peroxiredoxins (Prdx1-6), the glutaredoxins (Glrx1, 2, 3 and 5), thioredoxin (Txn1 and 2) and their reductases (Txnrd1 and 2) are expressed in neurons, glial and/or vascular cells of the dorsal root ganglia (DRGs) and in the spinal cord. They show distinct cellular and subcellular locations in agreement with the GO terms for "cellular component". The expression and localization of Glrx, Txn and Txnrd proteins was not affected by sciatic nerve injury but peroxiredoxins were upregulated in the DRGs, Prdx1 and Prdx6 mainly in non-neuronal cells and Prdx4 and Prdx5 in DRG neurons, the latter associated with an increase of respective mRNAs and protein accumulation in peripheral and/or central fibers. The upregulation of Prdx4 and Prdx5 in DRG neurons was reduced in mice with a cre-loxP mediated deficiency of hypoxia inducible factor 1 alpha (HIF1α) in these neurons. The results identify Prdx4 and Prdx5 as endogenous HIF1α-dependent, transcriptionally regulated defenders of nerve injury evoked redox stress that may be important for neuronal survival and regeneration.
DOI: 10.1016/j.freeradbiomed.2015.09.008
PubMed: 26456799
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Electronic address: tegeder@em.uni-frankfurt.de.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Clinical Pharmacology, Goethe-University Hospital, Frankfurt</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Disease Models, Animal (MeSH)</term><term>Female (MeSH)</term><term>Ganglia, Spinal (metabolism)</term><term>Ganglia, Spinal (pathology)</term><term>Glutaredoxins (biosynthesis)</term><term>Immunohistochemistry (MeSH)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Neuroglia (metabolism)</term><term>Neuroglia (pathology)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Oxidation-Reduction (MeSH)</term><term>Peroxiredoxins (biosynthesis)</term><term>RNA, Messenger (analysis)</term><term>Reverse Transcriptase Polymerase Chain Reaction (MeSH)</term><term>Sciatic Nerve (injuries)</term><term>Sciatic Neuropathy (metabolism)</term><term>Sciatic Neuropathy (pathology)</term><term>Thioredoxins (biosynthesis)</term><term>Up-Regulation (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (analyse)</term><term>Animaux (MeSH)</term><term>Femelle (MeSH)</term><term>Ganglions sensitifs des nerfs spinaux (anatomopathologie)</term><term>Ganglions sensitifs des nerfs spinaux (métabolisme)</term><term>Glutarédoxines (biosynthèse)</term><term>Immunohistochimie (MeSH)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Mâle (MeSH)</term><term>Nerf ischiatique (traumatismes)</term><term>Neurones (anatomopathologie)</term><term>Neurones (métabolisme)</term><term>Neuropathie du nerf sciatique (anatomopathologie)</term><term>Neuropathie du nerf sciatique (métabolisme)</term><term>Névroglie (anatomopathologie)</term><term>Névroglie (métabolisme)</term><term>Oxydoréduction (MeSH)</term><term>Peroxirédoxines (biosynthèse)</term><term>RT-PCR (MeSH)</term><term>Régulation positive (MeSH)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Thiorédoxines (biosynthèse)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Glutaredoxins</term><term>Peroxiredoxins</term><term>Thioredoxins</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>ARN messager</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Ganglions sensitifs des nerfs spinaux</term><term>Neurones</term><term>Neuropathie du nerf sciatique</term><term>Névroglie</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Glutarédoxines</term><term>Peroxirédoxines</term><term>Thiorédoxines</term></keywords><keywords scheme="MESH" qualifier="injuries" xml:lang="en"><term>Sciatic Nerve</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Ganglia, Spinal</term><term>Neuroglia</term><term>Neurons</term><term>Sciatic Neuropathy</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Ganglions sensitifs des nerfs spinaux</term><term>Neurones</term><term>Neuropathie du nerf sciatique</term><term>Névroglie</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Ganglia, Spinal</term><term>Neuroglia</term><term>Neurons</term><term>Sciatic Neuropathy</term></keywords><keywords scheme="MESH" qualifier="traumatismes" xml:lang="fr"><term>Nerf ischiatique</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Immunohistochemistry</term><term>Male</term><term>Mice</term><term>Mice, Knockout</term><term>Oxidation-Reduction</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Immunohistochimie</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Oxydoréduction</term><term>RT-PCR</term><term>Régulation positive</term><term>Souris</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Peripheral nerve injury causes redox stress in injured neurons by upregulations of pro-oxidative enzymes, but most neurons survive suggesting an activation of endogenous defense against the imbalance. As potential candidates we assessed thioredoxin-fold proteins, called redoxins, which maintain redox homeostasis by reduction of hydrogen peroxide or protein dithiol-disulfide exchange. Using a histologic approach, we show that the peroxiredoxins (Prdx1-6), the glutaredoxins (Glrx1, 2, 3 and 5), thioredoxin (Txn1 and 2) and their reductases (Txnrd1 and 2) are expressed in neurons, glial and/or vascular cells of the dorsal root ganglia (DRGs) and in the spinal cord. They show distinct cellular and subcellular locations in agreement with the GO terms for "cellular component". The expression and localization of Glrx, Txn and Txnrd proteins was not affected by sciatic nerve injury but peroxiredoxins were upregulated in the DRGs, Prdx1 and Prdx6 mainly in non-neuronal cells and Prdx4 and Prdx5 in DRG neurons, the latter associated with an increase of respective mRNAs and protein accumulation in peripheral and/or central fibers. The upregulation of Prdx4 and Prdx5 in DRG neurons was reduced in mice with a cre-loxP mediated deficiency of hypoxia inducible factor 1 alpha (HIF1α) in these neurons. The results identify Prdx4 and Prdx5 as endogenous HIF1α-dependent, transcriptionally regulated defenders of nerve injury evoked redox stress that may be important for neuronal survival and regeneration. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26456799</PMID><DateCompleted><Year>2016</Year><Month>09</Month><Day>21</Day></DateCompleted><DateRevised><Year>2015</Year><Month>12</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN><JournalIssue CitedMedium="Internet"><Volume>89</Volume><PubDate><Year>2015</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation></Journal><ArticleTitle>Redoxins in peripheral neurons after sciatic nerve injury.</ArticleTitle><Pagination><MedlinePgn>581-92</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2015.09.008</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0891-5849(15)00577-8</ELocationID><Abstract><AbstractText>Peripheral nerve injury causes redox stress in injured neurons by upregulations of pro-oxidative enzymes, but most neurons survive suggesting an activation of endogenous defense against the imbalance. As potential candidates we assessed thioredoxin-fold proteins, called redoxins, which maintain redox homeostasis by reduction of hydrogen peroxide or protein dithiol-disulfide exchange. Using a histologic approach, we show that the peroxiredoxins (Prdx1-6), the glutaredoxins (Glrx1, 2, 3 and 5), thioredoxin (Txn1 and 2) and their reductases (Txnrd1 and 2) are expressed in neurons, glial and/or vascular cells of the dorsal root ganglia (DRGs) and in the spinal cord. They show distinct cellular and subcellular locations in agreement with the GO terms for "cellular component". The expression and localization of Glrx, Txn and Txnrd proteins was not affected by sciatic nerve injury but peroxiredoxins were upregulated in the DRGs, Prdx1 and Prdx6 mainly in non-neuronal cells and Prdx4 and Prdx5 in DRG neurons, the latter associated with an increase of respective mRNAs and protein accumulation in peripheral and/or central fibers. The upregulation of Prdx4 and Prdx5 in DRG neurons was reduced in mice with a cre-loxP mediated deficiency of hypoxia inducible factor 1 alpha (HIF1α) in these neurons. The results identify Prdx4 and Prdx5 as endogenous HIF1α-dependent, transcriptionally regulated defenders of nerve injury evoked redox stress that may be important for neuronal survival and regeneration. </AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Valek</LastName><ForeName>Lucie</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Goethe-University Hospital, Frankfurt, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kanngießer</LastName><ForeName>Maike</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Goethe-University Hospital, Frankfurt, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Häussler</LastName><ForeName>Annett</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Goethe-University Hospital, Frankfurt, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Agarwal</LastName><ForeName>Nitin</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Institute of Pharmacology, Medical Faculty, University of Heidelberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lillig</LastName><ForeName>Christopher Horst</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>Institute for Medical Biochemistry and Molecular Biology, Medical Faculty of the Ernst-Moritz Arndt-University, Greifswald, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tegeder</LastName><ForeName>Irmgard</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Goethe-University Hospital, Frankfurt, Germany. Electronic address: tegeder@em.uni-frankfurt.de.</Affiliation></AffiliationInfo></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>2015</Year><Month>10</Month><Day>09</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="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>52500-60-4</RegistryNumber><NameOfSubstance UI="D013879">Thioredoxins</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="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005727" MajorTopicYN="N">Ganglia, Spinal</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009457" MajorTopicYN="N">Neuroglia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054464" MajorTopicYN="N">Peroxiredoxins</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012584" MajorTopicYN="N">Sciatic Nerve</DescriptorName><QualifierName UI="Q000293" MajorTopicYN="N">injuries</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020426" MajorTopicYN="N">Sciatic Neuropathy</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Axonal injury</Keyword><Keyword MajorTopicYN="N">Dorsal root ganglia</Keyword><Keyword MajorTopicYN="N">Glutathione</Keyword><Keyword MajorTopicYN="N">Hypoxia inducible factor 1 alpha</Keyword><Keyword MajorTopicYN="N">Redox stress</Keyword><Keyword MajorTopicYN="N">Redoxin</Keyword><Keyword MajorTopicYN="N">Sensory neuron</Keyword><Keyword MajorTopicYN="N">Spinal cord</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>08</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>09</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>09</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>10</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>10</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>9</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26456799</ArticleId><ArticleId IdType="pii">S0891-5849(15)00577-8</ArticleId><ArticleId IdType="doi">10.1016/j.freeradbiomed.2015.09.008</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>District de Darmstadt</li><li>Hesse (Land)</li></region><settlement><li>Francfort-sur-le-Main</li></settlement></list><tree><country name="Allemagne"><region name="Hesse (Land)"><name sortKey="Valek, Lucie" sort="Valek, Lucie" uniqKey="Valek L" first="Lucie" last="Valek">Lucie Valek</name></region><name sortKey="Agarwal, Nitin" sort="Agarwal, Nitin" uniqKey="Agarwal N" first="Nitin" last="Agarwal">Nitin Agarwal</name><name sortKey="H Ussler, Annett" sort="H Ussler, Annett" uniqKey="H Ussler A" first="Annett" last="H Ussler">Annett H Ussler</name><name sortKey="Kanngie Er, Maike" sort="Kanngie Er, Maike" uniqKey="Kanngie Er M" first="Maike" last="Kanngie Er">Maike Kanngie Er</name><name sortKey="Lillig, Christopher Horst" sort="Lillig, Christopher Horst" uniqKey="Lillig C" first="Christopher Horst" last="Lillig">Christopher Horst Lillig</name><name sortKey="Tegeder, Irmgard" sort="Tegeder, Irmgard" uniqKey="Tegeder I" first="Irmgard" last="Tegeder">Irmgard Tegeder</name></country></tree></affiliations></record>Pour 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