Influenza virus infection induces metallothionein gene expression in the mouse liver and lung by overlapping but distinct molecular mechanisms.
Identifieur interne : 002C84 ( Main/Exploration ); précédent : 002C83; suivant : 002C85Influenza virus infection induces metallothionein gene expression in the mouse liver and lung by overlapping but distinct molecular mechanisms.
Auteurs : K. Ghoshal [États-Unis] ; S. Majumder ; Q. Zhu ; J. Hunzeker ; J. Datta ; M. Shah ; J F Sheridan ; S T JacobSource :
- Molecular and cellular biology [ 0270-7306 ] ; 2001.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Activation enzymatique, Animaux, Antioxydants (pharmacologie), Cytokines (biosynthèse), Données de séquences moléculaires, Facteur de transcription STAT-1, Facteur de transcription STAT-3, Facteurs de transcription (métabolisme), Facteurs temps, Foie (métabolisme), Interféron gamma (biosynthèse), Interleukine-10 (biosynthèse), Interleukine-6 (métabolisme), Mifépristone (pharmacologie), Modèles biologiques, Mâle, Métallothionéine (biosynthèse), Noyau de la cellule (métabolisme), Orthomyxoviridae (métabolisme), Poumon (métabolisme), Protéines de liaison à l'ADN (métabolisme), Réaction de polymérisation en chaîne, Récepteurs aux glucocorticoïdes (antagonistes et inhibiteurs), Récepteurs aux glucocorticoïdes (métabolisme), Régions promotrices (génétique), Sites de fixation, Souris, Souris de lignée C57BL, Souris knockout, Stress oxydatif, Séquence nucléotidique, Technique de Northern, Transactivateurs (métabolisme).
- MESH :
- antagonistes et inhibiteurs : Récepteurs aux glucocorticoïdes.
- biosynthèse : Cytokines, Interféron gamma, Interleukine-10, Métallothionéine.
- métabolisme : ARN messager, Facteurs de transcription, Foie, Interleukine-6, Noyau de la cellule, Orthomyxoviridae, Poumon, Protéines de liaison à l'ADN, Récepteurs aux glucocorticoïdes, Transactivateurs.
- pharmacologie : Antioxydants, Mifépristone.
- Activation enzymatique, Animaux, Données de séquences moléculaires, Facteur de transcription STAT-1, Facteur de transcription STAT-3, Facteurs temps, Modèles biologiques, Mâle, Réaction de polymérisation en chaîne, Régions promotrices (génétique), Sites de fixation, Souris, Souris de lignée C57BL, Souris knockout, Stress oxydatif, Séquence nucléotidique, Technique de Northern.
English descriptors
- KwdEn :
- Animals, Antioxidants (pharmacology), Base Sequence, Binding Sites, Blotting, Northern, Cell Nucleus (metabolism), Cytokines (biosynthesis), DNA-Binding Proteins (metabolism), Enzyme Activation, Interferon-gamma (biosynthesis), Interleukin-10 (biosynthesis), Interleukin-6 (metabolism), Liver (metabolism), Lung (metabolism), Male, Metallothionein (biosynthesis), Mice, Mice, Inbred C57BL, Mice, Knockout, Mifepristone (pharmacology), Models, Biological, Molecular Sequence Data, Orthomyxoviridae (metabolism), Oxidative Stress, Polymerase Chain Reaction, Promoter Regions, Genetic, RNA, Messenger (metabolism), Receptors, Glucocorticoid (antagonists & inhibitors), Receptors, Glucocorticoid (metabolism), STAT1 Transcription Factor, STAT3 Transcription Factor, Time Factors, Trans-Activators (metabolism), Transcription Factors (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Receptors, Glucocorticoid.
- chemical , biosynthesis : Cytokines, Interferon-gamma, Interleukin-10, Metallothionein.
- chemical , metabolism : DNA-Binding Proteins, Interleukin-6, RNA, Messenger, Receptors, Glucocorticoid, Trans-Activators, Transcription Factors.
- chemical , pharmacology : Antioxidants, Mifepristone.
- metabolism : Cell Nucleus, Liver, Lung, Orthomyxoviridae.
- Animals, Base Sequence, Binding Sites, Blotting, Northern, Enzyme Activation, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Biological, Molecular Sequence Data, Oxidative Stress, Polymerase Chain Reaction, Promoter Regions, Genetic, STAT1 Transcription Factor, STAT3 Transcription Factor, Time Factors.
Abstract
Metallothionein I (MT-I) and MT-II have been implicated in the protection of cells against reactive oxygen species (ROS), heavy metals, and a variety of pathological and environmental stressors. Here, we show a robust increase in MT-I/MT-II mRNA level and MT proteins in the livers and lungs of C57BL/6 mice exposed to the influenza A/PR8 virus that infects the upper respiratory tract and lungs. Interleukin-6 (IL-6) had a pronounced effect on the induction of these genes in the liver but not the lung. Treatment of the animals with RU-486, a glucocorticoid receptor antagonist, inhibited induction of MT-I/MT-II in both liver and lung, revealing a direct role of glucocorticoid that is increased upon infection in this induction process. In vivo genomic footprinting (IVGF) analysis demonstrated involvement of almost all metal response elements, major late transcription factor/antioxidant response element (MLTF/ARE), the STAT3 binding site on the MT-I upstream promoter, and the glucocorticoid responsive element (GRE1), located upstream of the MT-II gene, in the induction process in the liver and lung. In the lung, inducible footprinting was also identified at a unique gamma interferon (IFN-gamma) response element (gamma-IRE) and at Sp1 sites. The mobility shift analysis showed activation of STAT3 and the glucocorticoid receptor in the liver and lung nuclear extracts, which was consistent with the IVGF data. Analysis of the newly synthesized mRNA for cytokines in the infected lung by real-time PCR showed a robust increase in the levels of IL-10 and IFN-gamma mRNA that can activate STAT3 and STAT1, respectively. A STAT1-containing complex that binds to the gamma-IRE in vitro was activated in the infected lung. No major change in MLTF/ARE DNA binding activity in the liver and lung occurred after infection. These results have demonstrated that MT-I and MT-II can be induced robustly in the liver and lung following experimental influenza virus infection by overlapping but distinct molecular mechanisms.
DOI: 10.1128/MCB.21.24.8301-8317.2001
PubMed: 11713267
Affiliations:
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Le document en format XML
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<affiliation wicri:level="2"><nlm:affiliation>Department of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, 333 Hamilton Hall, 1645 Neil Ave., Columbus, OH 43210, USA.</nlm:affiliation>
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<author><name sortKey="Hunzeker, J" sort="Hunzeker, J" uniqKey="Hunzeker J" first="J" last="Hunzeker">J. Hunzeker</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Influenza virus infection induces metallothionein gene expression in the mouse liver and lung by overlapping but distinct molecular mechanisms.</title>
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<wicri:regionArea>Department of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, 333 Hamilton Hall, 1645 Neil Ave., Columbus, OH 43210</wicri:regionArea>
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<term>Antioxidants (pharmacology)</term>
<term>Base Sequence</term>
<term>Binding Sites</term>
<term>Blotting, Northern</term>
<term>Cell Nucleus (metabolism)</term>
<term>Cytokines (biosynthesis)</term>
<term>DNA-Binding Proteins (metabolism)</term>
<term>Enzyme Activation</term>
<term>Interferon-gamma (biosynthesis)</term>
<term>Interleukin-10 (biosynthesis)</term>
<term>Interleukin-6 (metabolism)</term>
<term>Liver (metabolism)</term>
<term>Lung (metabolism)</term>
<term>Male</term>
<term>Metallothionein (biosynthesis)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Mifepristone (pharmacology)</term>
<term>Models, Biological</term>
<term>Molecular Sequence Data</term>
<term>Orthomyxoviridae (metabolism)</term>
<term>Oxidative Stress</term>
<term>Polymerase Chain Reaction</term>
<term>Promoter Regions, Genetic</term>
<term>RNA, Messenger (metabolism)</term>
<term>Receptors, Glucocorticoid (antagonists & inhibitors)</term>
<term>Receptors, Glucocorticoid (metabolism)</term>
<term>STAT1 Transcription Factor</term>
<term>STAT3 Transcription Factor</term>
<term>Time Factors</term>
<term>Trans-Activators (metabolism)</term>
<term>Transcription Factors (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term>
<term>Activation enzymatique</term>
<term>Animaux</term>
<term>Antioxydants (pharmacologie)</term>
<term>Cytokines (biosynthèse)</term>
<term>Données de séquences moléculaires</term>
<term>Facteur de transcription STAT-1</term>
<term>Facteur de transcription STAT-3</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Facteurs temps</term>
<term>Foie (métabolisme)</term>
<term>Interféron gamma (biosynthèse)</term>
<term>Interleukine-10 (biosynthèse)</term>
<term>Interleukine-6 (métabolisme)</term>
<term>Mifépristone (pharmacologie)</term>
<term>Modèles biologiques</term>
<term>Mâle</term>
<term>Métallothionéine (biosynthèse)</term>
<term>Noyau de la cellule (métabolisme)</term>
<term>Orthomyxoviridae (métabolisme)</term>
<term>Poumon (métabolisme)</term>
<term>Protéines de liaison à l'ADN (métabolisme)</term>
<term>Réaction de polymérisation en chaîne</term>
<term>Récepteurs aux glucocorticoïdes (antagonistes et inhibiteurs)</term>
<term>Récepteurs aux glucocorticoïdes (métabolisme)</term>
<term>Régions promotrices (génétique)</term>
<term>Sites de fixation</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Stress oxydatif</term>
<term>Séquence nucléotidique</term>
<term>Technique de Northern</term>
<term>Transactivateurs (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, Glucocorticoid</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term>
<term>Interferon-gamma</term>
<term>Interleukin-10</term>
<term>Metallothionein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>DNA-Binding Proteins</term>
<term>Interleukin-6</term>
<term>RNA, Messenger</term>
<term>Receptors, Glucocorticoid</term>
<term>Trans-Activators</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antioxidants</term>
<term>Mifepristone</term>
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<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteurs aux glucocorticoïdes</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Cytokines</term>
<term>Interféron gamma</term>
<term>Interleukine-10</term>
<term>Métallothionéine</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cell Nucleus</term>
<term>Liver</term>
<term>Lung</term>
<term>Orthomyxoviridae</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term>
<term>Facteurs de transcription</term>
<term>Foie</term>
<term>Interleukine-6</term>
<term>Noyau de la cellule</term>
<term>Orthomyxoviridae</term>
<term>Poumon</term>
<term>Protéines de liaison à l'ADN</term>
<term>Récepteurs aux glucocorticoïdes</term>
<term>Transactivateurs</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antioxydants</term>
<term>Mifépristone</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Base Sequence</term>
<term>Binding Sites</term>
<term>Blotting, Northern</term>
<term>Enzyme Activation</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Models, Biological</term>
<term>Molecular Sequence Data</term>
<term>Oxidative Stress</term>
<term>Polymerase Chain Reaction</term>
<term>Promoter Regions, Genetic</term>
<term>STAT1 Transcription Factor</term>
<term>STAT3 Transcription Factor</term>
<term>Time Factors</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Activation enzymatique</term>
<term>Animaux</term>
<term>Données de séquences moléculaires</term>
<term>Facteur de transcription STAT-1</term>
<term>Facteur de transcription STAT-3</term>
<term>Facteurs temps</term>
<term>Modèles biologiques</term>
<term>Mâle</term>
<term>Réaction de polymérisation en chaîne</term>
<term>Régions promotrices (génétique)</term>
<term>Sites de fixation</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Stress oxydatif</term>
<term>Séquence nucléotidique</term>
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<front><div type="abstract" xml:lang="en">Metallothionein I (MT-I) and MT-II have been implicated in the protection of cells against reactive oxygen species (ROS), heavy metals, and a variety of pathological and environmental stressors. Here, we show a robust increase in MT-I/MT-II mRNA level and MT proteins in the livers and lungs of C57BL/6 mice exposed to the influenza A/PR8 virus that infects the upper respiratory tract and lungs. Interleukin-6 (IL-6) had a pronounced effect on the induction of these genes in the liver but not the lung. Treatment of the animals with RU-486, a glucocorticoid receptor antagonist, inhibited induction of MT-I/MT-II in both liver and lung, revealing a direct role of glucocorticoid that is increased upon infection in this induction process. In vivo genomic footprinting (IVGF) analysis demonstrated involvement of almost all metal response elements, major late transcription factor/antioxidant response element (MLTF/ARE), the STAT3 binding site on the MT-I upstream promoter, and the glucocorticoid responsive element (GRE1), located upstream of the MT-II gene, in the induction process in the liver and lung. In the lung, inducible footprinting was also identified at a unique gamma interferon (IFN-gamma) response element (gamma-IRE) and at Sp1 sites. The mobility shift analysis showed activation of STAT3 and the glucocorticoid receptor in the liver and lung nuclear extracts, which was consistent with the IVGF data. Analysis of the newly synthesized mRNA for cytokines in the infected lung by real-time PCR showed a robust increase in the levels of IL-10 and IFN-gamma mRNA that can activate STAT3 and STAT1, respectively. A STAT1-containing complex that binds to the gamma-IRE in vitro was activated in the infected lung. No major change in MLTF/ARE DNA binding activity in the liver and lung occurred after infection. These results have demonstrated that MT-I and MT-II can be induced robustly in the liver and lung following experimental influenza virus infection by overlapping but distinct molecular mechanisms.</div>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Ohio</li>
</region>
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<tree><noCountry><name sortKey="Datta, J" sort="Datta, J" uniqKey="Datta J" first="J" last="Datta">J. Datta</name>
<name sortKey="Hunzeker, J" sort="Hunzeker, J" uniqKey="Hunzeker J" first="J" last="Hunzeker">J. Hunzeker</name>
<name sortKey="Jacob, S T" sort="Jacob, S T" uniqKey="Jacob S" first="S T" last="Jacob">S T Jacob</name>
<name sortKey="Majumder, S" sort="Majumder, S" uniqKey="Majumder S" first="S" last="Majumder">S. Majumder</name>
<name sortKey="Shah, M" sort="Shah, M" uniqKey="Shah M" first="M" last="Shah">M. Shah</name>
<name sortKey="Sheridan, J F" sort="Sheridan, J F" uniqKey="Sheridan J" first="J F" last="Sheridan">J F Sheridan</name>
<name sortKey="Zhu, Q" sort="Zhu, Q" uniqKey="Zhu Q" first="Q" last="Zhu">Q. Zhu</name>
</noCountry>
<country name="États-Unis"><region name="Ohio"><name sortKey="Ghoshal, K" sort="Ghoshal, K" uniqKey="Ghoshal K" first="K" last="Ghoshal">K. Ghoshal</name>
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