Differential expression of glutaredoxin and thioredoxin during monocytic differentiation.
Identifieur interne : 001109 ( Main/Exploration ); précédent : 001108; suivant : 001110Differential expression of glutaredoxin and thioredoxin during monocytic differentiation.
Auteurs : Y. Takashima [Japon] ; K. Hirota ; H. Nakamura ; T. Nakamura ; K. Akiyama ; F S Cheng ; M. Maeda ; J. YodoiSource :
- Immunology letters [ 0165-2478 ] ; 1999.
Descripteurs français
- KwdFr :
- ARN messager (analyse), Animaux (MeSH), Biosynthèse des protéines (MeSH), Cellules U937 (MeSH), Cellules cancéreuses en culture (MeSH), Différenciation cellulaire (MeSH), Glutarédoxines (MeSH), Humains (MeSH), Interleukine-6 (pharmacologie), Macrophages (cytologie), Macrophages (effets des médicaments et des substances chimiques), Monocytes (cytologie), Monocytes (effets des médicaments et des substances chimiques), Oxidoreductases (MeSH), Peroxyde d'hydrogène (métabolisme), Protéines (génétique), Souris (MeSH), Thiorédoxines (biosynthèse), Thiorédoxines (génétique).
- MESH :
- analyse : ARN messager.
- biosynthèse : Thiorédoxines.
- cytologie : Macrophages, Monocytes.
- effets des médicaments et des substances chimiques : Macrophages, Monocytes.
- génétique : Protéines, Thiorédoxines.
- métabolisme : Peroxyde d'hydrogène.
- pharmacologie : Interleukine-6.
- Animaux, Biosynthèse des protéines, Cellules U937, Cellules cancéreuses en culture, Différenciation cellulaire, Glutarédoxines, Humains, Oxidoreductases, Souris.
English descriptors
- KwdEn :
- Animals (MeSH), Cell Differentiation (MeSH), Glutaredoxins (MeSH), Humans (MeSH), Hydrogen Peroxide (metabolism), Interleukin-6 (pharmacology), Macrophages (cytology), Macrophages (drug effects), Mice (MeSH), Monocytes (cytology), Monocytes (drug effects), Oxidoreductases (MeSH), Protein Biosynthesis (MeSH), Proteins (genetics), RNA, Messenger (analysis), Thioredoxins (biosynthesis), Thioredoxins (genetics), Tumor Cells, Cultured (MeSH), U937 Cells (MeSH).
- MESH :
- chemical , analysis : RNA, Messenger.
- chemical , biosynthesis : Thioredoxins.
- chemical , genetics : Proteins, Thioredoxins.
- chemical , metabolism : Hydrogen Peroxide.
- chemical , pharmacology : Interleukin-6.
- chemical : Glutaredoxins, Oxidoreductases.
- cytology : Macrophages, Monocytes.
- drug effects : Macrophages, Monocytes.
- Animals, Cell Differentiation, Humans, Mice, Protein Biosynthesis, Tumor Cells, Cultured, U937 Cells.
Abstract
Macrophages generate reactive oxygen intermediates (ROIs) as the effectors of anti-bacterial defense mechanism. Intracellular ROIs and reduction/oxidation (redox) status play crucial roles in signal transduction. We therefore investigated the expression of redox-regulating proteins such as glutaredoxin (GRX) and thioredoxin (TRX) during the differentiation of murine monocytic leukemia cell line M1 cells and human monocytic leukemia cell line U937 cells. When M1 cells were treated by IL-6, GRX mRNA markedly increased and TRX mRNA also increased slightly. In contrast, there was no increase of GRX mRNA in D-cell, which is a sub-cell line derived from M1 lacking in the capacity of differentiation. GRX mRNA also increased in U937 cells differentiated by phorbol 12-myristate 13-acetate (PMA). By immunohistochemistry, unstimulated M1 cells showed strong staining of TRX and marginal staining of GRX. In contrast, TRX expression in IL-6 treated M1 cells is as strong as in unstimulated M1 cells, whereas GRX expression is slightly enhanced in IL-6 treated M1 cells. Phagocytosis is markedly enhanced and hydrogen peroxide production is slightly enhanced in IL-6 treated M1 cells. These results showed that TRX is steadily expressed whereas GRX is induced in association with the differentiation in macrophage-like cell line cells, suggesting differential roles of these redox regulators in macrophage lineage.
DOI: 10.1016/s0165-2478(99)00087-5
PubMed: 10424449
Affiliations:
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Hirota</name></author><author><name sortKey="Nakamura, H" sort="Nakamura, H" uniqKey="Nakamura H" first="H" last="Nakamura">H. Nakamura</name></author><author><name sortKey="Nakamura, T" sort="Nakamura, T" uniqKey="Nakamura T" first="T" last="Nakamura">T. Nakamura</name></author><author><name sortKey="Akiyama, K" sort="Akiyama, K" uniqKey="Akiyama K" first="K" last="Akiyama">K. Akiyama</name></author><author><name sortKey="Cheng, F S" sort="Cheng, F S" uniqKey="Cheng F" first="F S" last="Cheng">F S Cheng</name></author><author><name sortKey="Maeda, M" sort="Maeda, M" uniqKey="Maeda M" first="M" last="Maeda">M. Maeda</name></author><author><name sortKey="Yodoi, J" sort="Yodoi, J" uniqKey="Yodoi J" first="J" last="Yodoi">J. Yodoi</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1999">1999</date><idno type="RBID">pubmed:10424449</idno><idno type="pmid">10424449</idno><idno type="doi">10.1016/s0165-2478(99)00087-5</idno><idno type="wicri:Area/Main/Corpus">001103</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001103</idno><idno type="wicri:Area/Main/Curation">001103</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">001103</idno><idno type="wicri:Area/Main/Exploration">001103</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Differential expression of glutaredoxin and thioredoxin during monocytic differentiation.</title><author><name sortKey="Takashima, Y" sort="Takashima, Y" uniqKey="Takashima Y" first="Y" last="Takashima">Y. Takashima</name><affiliation wicri:level="4"><nlm:affiliation>Department of Biological Responses, Institute for Virus Research, Kyoto University, Sakyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Biological Responses, Institute for Virus Research, Kyoto University, Sakyo</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Hirota, K" sort="Hirota, K" uniqKey="Hirota K" first="K" last="Hirota">K. Hirota</name></author><author><name sortKey="Nakamura, H" sort="Nakamura, H" uniqKey="Nakamura H" first="H" last="Nakamura">H. Nakamura</name></author><author><name sortKey="Nakamura, T" sort="Nakamura, T" uniqKey="Nakamura T" first="T" last="Nakamura">T. Nakamura</name></author><author><name sortKey="Akiyama, K" sort="Akiyama, K" uniqKey="Akiyama K" first="K" last="Akiyama">K. Akiyama</name></author><author><name sortKey="Cheng, F S" sort="Cheng, F S" uniqKey="Cheng F" first="F S" last="Cheng">F S Cheng</name></author><author><name sortKey="Maeda, M" sort="Maeda, M" uniqKey="Maeda M" first="M" last="Maeda">M. Maeda</name></author><author><name sortKey="Yodoi, J" sort="Yodoi, J" uniqKey="Yodoi J" first="J" last="Yodoi">J. Yodoi</name></author></analytic><series><title level="j">Immunology letters</title><idno type="ISSN">0165-2478</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cell Differentiation (MeSH)</term><term>Glutaredoxins (MeSH)</term><term>Humans (MeSH)</term><term>Hydrogen Peroxide (metabolism)</term><term>Interleukin-6 (pharmacology)</term><term>Macrophages (cytology)</term><term>Macrophages (drug effects)</term><term>Mice (MeSH)</term><term>Monocytes (cytology)</term><term>Monocytes (drug effects)</term><term>Oxidoreductases (MeSH)</term><term>Protein Biosynthesis (MeSH)</term><term>Proteins (genetics)</term><term>RNA, Messenger (analysis)</term><term>Thioredoxins (biosynthesis)</term><term>Thioredoxins (genetics)</term><term>Tumor Cells, Cultured (MeSH)</term><term>U937 Cells (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (analyse)</term><term>Animaux (MeSH)</term><term>Biosynthèse des protéines (MeSH)</term><term>Cellules U937 (MeSH)</term><term>Cellules cancéreuses en culture (MeSH)</term><term>Différenciation cellulaire (MeSH)</term><term>Glutarédoxines (MeSH)</term><term>Humains (MeSH)</term><term>Interleukine-6 (pharmacologie)</term><term>Macrophages (cytologie)</term><term>Macrophages (effets des médicaments et des substances chimiques)</term><term>Monocytes (cytologie)</term><term>Monocytes (effets des médicaments et des substances chimiques)</term><term>Oxidoreductases (MeSH)</term><term>Peroxyde d'hydrogène (métabolisme)</term><term>Protéines (génétique)</term><term>Souris (MeSH)</term><term>Thiorédoxines (biosynthèse)</term><term>Thiorédoxines (génétique)</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>Thioredoxins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Proteins</term><term>Thioredoxins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hydrogen Peroxide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Interleukin-6</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Glutaredoxins</term><term>Oxidoreductases</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>ARN messager</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Thiorédoxines</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Macrophages</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Macrophages</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Macrophages</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Macrophages</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines</term><term>Thiorédoxines</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Peroxyde d'hydrogène</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Interleukine-6</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Differentiation</term><term>Humans</term><term>Mice</term><term>Protein Biosynthesis</term><term>Tumor Cells, Cultured</term><term>U937 Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Biosynthèse des protéines</term><term>Cellules U937</term><term>Cellules cancéreuses en culture</term><term>Différenciation cellulaire</term><term>Glutarédoxines</term><term>Humains</term><term>Oxidoreductases</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Macrophages generate reactive oxygen intermediates (ROIs) as the effectors of anti-bacterial defense mechanism. Intracellular ROIs and reduction/oxidation (redox) status play crucial roles in signal transduction. We therefore investigated the expression of redox-regulating proteins such as glutaredoxin (GRX) and thioredoxin (TRX) during the differentiation of murine monocytic leukemia cell line M1 cells and human monocytic leukemia cell line U937 cells. When M1 cells were treated by IL-6, GRX mRNA markedly increased and TRX mRNA also increased slightly. In contrast, there was no increase of GRX mRNA in D-cell, which is a sub-cell line derived from M1 lacking in the capacity of differentiation. GRX mRNA also increased in U937 cells differentiated by phorbol 12-myristate 13-acetate (PMA). By immunohistochemistry, unstimulated M1 cells showed strong staining of TRX and marginal staining of GRX. In contrast, TRX expression in IL-6 treated M1 cells is as strong as in unstimulated M1 cells, whereas GRX expression is slightly enhanced in IL-6 treated M1 cells. Phagocytosis is markedly enhanced and hydrogen peroxide production is slightly enhanced in IL-6 treated M1 cells. These results showed that TRX is steadily expressed whereas GRX is induced in association with the differentiation in macrophage-like cell line cells, suggesting differential roles of these redox regulators in macrophage lineage.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10424449</PMID><DateCompleted><Year>1999</Year><Month>09</Month><Day>16</Day></DateCompleted><DateRevised><Year>2019</Year><Month>08</Month><Day>26</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0165-2478</ISSN><JournalIssue CitedMedium="Print"><Volume>68</Volume><Issue>2-3</Issue><PubDate><Year>1999</Year><Month>Jun</Month><Day>01</Day></PubDate></JournalIssue><Title>Immunology letters</Title><ISOAbbreviation>Immunol Lett</ISOAbbreviation></Journal><ArticleTitle>Differential expression of glutaredoxin and thioredoxin during monocytic differentiation.</ArticleTitle><Pagination><MedlinePgn>397-401</MedlinePgn></Pagination><Abstract><AbstractText>Macrophages generate reactive oxygen intermediates (ROIs) as the effectors of anti-bacterial defense mechanism. Intracellular ROIs and reduction/oxidation (redox) status play crucial roles in signal transduction. We therefore investigated the expression of redox-regulating proteins such as glutaredoxin (GRX) and thioredoxin (TRX) during the differentiation of murine monocytic leukemia cell line M1 cells and human monocytic leukemia cell line U937 cells. When M1 cells were treated by IL-6, GRX mRNA markedly increased and TRX mRNA also increased slightly. In contrast, there was no increase of GRX mRNA in D-cell, which is a sub-cell line derived from M1 lacking in the capacity of differentiation. GRX mRNA also increased in U937 cells differentiated by phorbol 12-myristate 13-acetate (PMA). By immunohistochemistry, unstimulated M1 cells showed strong staining of TRX and marginal staining of GRX. In contrast, TRX expression in IL-6 treated M1 cells is as strong as in unstimulated M1 cells, whereas GRX expression is slightly enhanced in IL-6 treated M1 cells. Phagocytosis is markedly enhanced and hydrogen peroxide production is slightly enhanced in IL-6 treated M1 cells. These results showed that TRX is steadily expressed whereas GRX is induced in association with the differentiation in macrophage-like cell line cells, suggesting differential roles of these redox regulators in macrophage lineage.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Takashima</LastName><ForeName>Y</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Biological Responses, Institute for Virus Research, Kyoto University, Sakyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hirota</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Nakamura</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Nakamura</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Akiyama</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>F S</ForeName><Initials>FS</Initials></Author><Author ValidYN="Y"><LastName>Maeda</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Yodoi</LastName><ForeName>J</ForeName><Initials>J</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></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Immunol Lett</MedlineTA><NlmUniqueID>7910006</NlmUniqueID><ISSNLinking>0165-2478</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516005">GLRX protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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MajorTopicYN="N">Cell Differentiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009000" MajorTopicYN="N">Monocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010088" MajorTopicYN="Y">Oxidoreductases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014176" MajorTopicYN="Y">Protein Biosynthesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011506" MajorTopicYN="N">Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014407" MajorTopicYN="N">Tumor Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020298" MajorTopicYN="N">U937 Cells</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>7</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>7</Month><Day>29</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>7</Month><Day>29</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10424449</ArticleId><ArticleId IdType="pii">S0165-2478(99)00087-5</ArticleId><ArticleId IdType="doi">10.1016/s0165-2478(99)00087-5</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country><region><li>Région du Kansai</li></region><settlement><li>Kyoto</li></settlement><orgName><li>Université de Kyoto</li></orgName></list><tree><noCountry><name sortKey="Akiyama, K" sort="Akiyama, K" uniqKey="Akiyama K" first="K" last="Akiyama">K. Akiyama</name><name sortKey="Cheng, F S" sort="Cheng, F S" uniqKey="Cheng F" first="F S" last="Cheng">F S Cheng</name><name sortKey="Hirota, K" sort="Hirota, K" uniqKey="Hirota K" first="K" last="Hirota">K. Hirota</name><name sortKey="Maeda, M" sort="Maeda, M" uniqKey="Maeda M" first="M" last="Maeda">M. Maeda</name><name sortKey="Nakamura, H" sort="Nakamura, H" uniqKey="Nakamura H" first="H" last="Nakamura">H. Nakamura</name><name sortKey="Nakamura, T" sort="Nakamura, T" uniqKey="Nakamura T" first="T" last="Nakamura">T. Nakamura</name><name sortKey="Yodoi, J" sort="Yodoi, J" uniqKey="Yodoi J" first="J" last="Yodoi">J. Yodoi</name></noCountry><country name="Japon"><region name="Région du Kansai"><name sortKey="Takashima, Y" sort="Takashima, Y" uniqKey="Takashima Y" first="Y" last="Takashima">Y. Takashima</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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