DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.
Identifieur interne : 000D21 ( Main/Exploration ); précédent : 000D20; suivant : 000D22DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.
Auteurs : Yan Ye [États-Unis] ; Ping Lin [États-Unis] ; Weidong Zhang [États-Unis] ; Shirui Tan [États-Unis] ; Xikun Zhou [États-Unis] ; Rongpeng Li [États-Unis] ; Qinqin Pu [États-Unis] ; Jonathan L. Koff [États-Unis] ; Archana Dhasarathy [États-Unis] ; Feng Ma [Japon] ; Xin Deng [Japon] ; Jianxin Jiang [Japon] ; Min Wu [Japon]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Autophagie, Cytokines (biosynthèse), DNA Glycosylases (métabolisme), Hyperoxie (anatomopathologie), Hyperoxie (métabolisme), Immunoprécipitation, Immunoprécipitation de la chromatine, Inflammation (anatomopathologie), Inflammation (métabolisme), Lésion pulmonaire aigüe (anatomopathologie), Lésion pulmonaire aigüe (métabolisme), Modèles animaux de maladie humaine, Poumon (anatomopathologie), Poumon (métabolisme), Réparation de l'ADN, Souris, Souris de lignée C57BL, Souris knockout, Technique de Western, Test des comètes.
- MESH :
- anatomopathologie : Hyperoxie, Inflammation, Lésion pulmonaire aigüe, Poumon.
- biosynthèse : Cytokines.
- métabolisme : DNA Glycosylases, Hyperoxie, Inflammation, Lésion pulmonaire aigüe, Poumon.
- Animaux, Autophagie, Immunoprécipitation, Immunoprécipitation de la chromatine, Modèles animaux de maladie humaine, Réparation de l'ADN, Souris, Souris de lignée C57BL, Souris knockout, Technique de Western, Test des comètes.
English descriptors
- KwdEn :
- Acute Lung Injury (metabolism), Acute Lung Injury (pathology), Animals, Autophagy, Blotting, Western, Chromatin Immunoprecipitation, Comet Assay, Cytokines (biosynthesis), DNA Glycosylases (metabolism), DNA Repair, Disease Models, Animal, Hyperoxia (metabolism), Hyperoxia (pathology), Immunoprecipitation, Inflammation (metabolism), Inflammation (pathology), Lung (metabolism), Lung (pathology), Mice, Mice, Inbred C57BL, Mice, Knockout.
- MESH :
- chemical , biosynthesis : Cytokines.
- metabolism : Acute Lung Injury, DNA Glycosylases, Hyperoxia, Inflammation, Lung.
- pathology : Acute Lung Injury, Hyperoxia, Inflammation, Lung.
- Animals, Autophagy, Blotting, Western, Chromatin Immunoprecipitation, Comet Assay, DNA Repair, Disease Models, Animal, Immunoprecipitation, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
Oxygen is supplied as a supportive treatment for patients suffering from acute respiratory distress syndrome. Unfortunately, high oxygen concentration increases reactive oxygen species generation, which causes DNA damage and ultimately cell death in the lung. Although 8-oxoguanine-DNA glycosylase (OGG-1) is involved in repairing hyperoxia-mediated DNA damage, the underlying molecular mechanism remains elusive. In this study, we report that ogg-1-deficient mice exhibited a significant increase of proinflammatory cytokines (TNF-α, IL-6, and IFN-γ) in the lung after being exposed to 95% oxygen. In addition, we found that ogg-1 deficiency downregulated (macro)autophagy when exposed to hyperoxia both in vitro and in vivo, which was evident by decreased conversion of LC3-I to LC3-II, reduced LC3 punctate staining, and lower Atg7 expression compared with controls. Using a chromatin immunoprecipitation assay, we found that OGG-1 associated with the promoter of Atg7, suggesting a role for OGG1 in regulation of Atg7 activity. Knocking down OGG-1 decreased the luciferase reporter activity of Atg7. Further, inflammatory cytokine levels in murine lung epithelial cell line cells were downregulated following autophagy induction by starvation and rapamycin treatment, and upregulated when autophagy was blocked using 3-methyladenine and chloroquine. atg7 knockout mice and Atg7 small interfering RNA-treated cells exhibited elevated levels of phospho-NF-κB and intensified inflammatory cytokines, suggesting that Atg7 impacts inflammatory responses to hyperoxia. These findings demonstrate that OGG-1 negatively regulates inflammatory cytokine release by coordinating molecular interaction with the autophagic pathway in hyperoxia-induced lung injury.
DOI: 10.4049/jimmunol.1601001
PubMed: 28202616
Affiliations:
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Dakota, Grand Forks, ND 58203.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Dakota du Nord</region></placeName><wicri:cityArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:cityArea></affiliation></author><author><name sortKey="Lin, Ping" sort="Lin, Ping" uniqKey="Lin P" first="Ping" last="Lin">Ping Lin</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Dakota du Nord</region></placeName><wicri:cityArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:cityArea></affiliation></author><author><name sortKey="Zhang, Weidong" sort="Zhang, Weidong" uniqKey="Zhang W" first="Weidong" last="Zhang">Weidong Zhang</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Dakota du Nord</region></placeName><wicri:cityArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:cityArea></affiliation></author><author><name sortKey="Tan, Shirui" sort="Tan, Shirui" uniqKey="Tan S" first="Shirui" last="Tan">Shirui Tan</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Dakota du Nord</region></placeName><wicri:cityArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:cityArea></affiliation></author><author><name sortKey="Zhou, Xikun" sort="Zhou, Xikun" uniqKey="Zhou X" first="Xikun" last="Zhou">Xikun Zhou</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Dakota du Nord</region></placeName><wicri:cityArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:cityArea></affiliation></author><author><name sortKey="Li, Rongpeng" sort="Li, Rongpeng" uniqKey="Li R" first="Rongpeng" last="Li">Rongpeng Li</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Dakota du Nord</region></placeName><wicri:cityArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:cityArea></affiliation></author><author><name sortKey="Pu, Qinqin" sort="Pu, Qinqin" uniqKey="Pu Q" first="Qinqin" last="Pu">Qinqin Pu</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Dakota du Nord</region></placeName><wicri:cityArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:cityArea></affiliation></author><author><name sortKey="Koff, Jonathan L" sort="Koff, Jonathan L" uniqKey="Koff J" first="Jonathan L" last="Koff">Jonathan L. Koff</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Yale University, New Haven, CT 06510.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Connecticut</region></placeName><wicri:cityArea>Department of Medicine, Yale University, New Haven</wicri:cityArea></affiliation></author><author><name sortKey="Dhasarathy, Archana" sort="Dhasarathy, Archana" uniqKey="Dhasarathy A" first="Archana" last="Dhasarathy">Archana Dhasarathy</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Dakota du Nord</region></placeName><wicri:cityArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:cityArea></affiliation></author><author><name sortKey="Ma, Feng" sort="Ma, Feng" uniqKey="Ma F" first="Feng" last="Ma">Feng Ma</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu 100005, People's Republic of China; and mafeng@hotmail.co.jp hellojjx@126.com xindeng@cityu.edu.hk.</nlm:affiliation><country wicri:rule="url">Japon</country><wicri:regionArea>Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu 100005</wicri:regionArea><wicri:noRegion>Chengdu 100005</wicri:noRegion></affiliation></author><author><name sortKey="Deng, Xin" sort="Deng, Xin" uniqKey="Deng X" first="Xin" last="Deng">Xin Deng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Sciences, City University of Hong Kong, Hong Kong 999077, People's Republic of China mafeng@hotmail.co.jp hellojjx@126.com xindeng@cityu.edu.hk.</nlm:affiliation><country wicri:rule="url">Japon</country><wicri:regionArea>Department of Biomedical Sciences, City University of Hong Kong, Hong Kong 999077</wicri:regionArea><wicri:noRegion>Hong Kong 999077</wicri:noRegion></affiliation></author><author><name sortKey="Jiang, Jianxin" sort="Jiang, Jianxin" uniqKey="Jiang J" first="Jianxin" last="Jiang">Jianxin Jiang</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, The Third Military Medical University, Chongqing 400042, People's Republic of China; mafeng@hotmail.co.jp hellojjx@126.com xindeng@cityu.edu.hk.</nlm:affiliation><country wicri:rule="url">Japon</country><wicri:regionArea>State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, The Third Military Medical University, Chongqing 400042</wicri:regionArea><wicri:noRegion>Chongqing 400042</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Min" sort="Wu, Min" uniqKey="Wu M" first="Min" last="Wu">Min Wu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203; mafeng@hotmail.co.jp hellojjx@126.com xindeng@cityu.edu.hk.</nlm:affiliation><country wicri:rule="url">Japon</country><wicri:regionArea>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks</wicri:regionArea><wicri:noRegion>Grand Forks</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="eISSN">1550-6606</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Lung Injury (metabolism)</term><term>Acute Lung Injury (pathology)</term><term>Animals</term><term>Autophagy</term><term>Blotting, Western</term><term>Chromatin Immunoprecipitation</term><term>Comet Assay</term><term>Cytokines (biosynthesis)</term><term>DNA Glycosylases (metabolism)</term><term>DNA Repair</term><term>Disease Models, Animal</term><term>Hyperoxia (metabolism)</term><term>Hyperoxia (pathology)</term><term>Immunoprecipitation</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Lung (metabolism)</term><term>Lung (pathology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Cytokines (biosynthèse)</term><term>DNA Glycosylases (métabolisme)</term><term>Hyperoxie (anatomopathologie)</term><term>Hyperoxie (métabolisme)</term><term>Immunoprécipitation</term><term>Immunoprécipitation de la chromatine</term><term>Inflammation (anatomopathologie)</term><term>Inflammation (métabolisme)</term><term>Lésion pulmonaire aigüe (anatomopathologie)</term><term>Lésion pulmonaire aigüe (métabolisme)</term><term>Modèles animaux de maladie humaine</term><term>Poumon (anatomopathologie)</term><term>Poumon (métabolisme)</term><term>Réparation de l'ADN</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Technique de Western</term><term>Test des comètes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hyperoxie</term><term>Inflammation</term><term>Lésion pulmonaire aigüe</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Acute Lung Injury</term><term>DNA Glycosylases</term><term>Hyperoxia</term><term>Inflammation</term><term>Lung</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>DNA Glycosylases</term><term>Hyperoxie</term><term>Inflammation</term><term>Lésion pulmonaire aigüe</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Acute Lung Injury</term><term>Hyperoxia</term><term>Inflammation</term><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autophagy</term><term>Blotting, Western</term><term>Chromatin Immunoprecipitation</term><term>Comet Assay</term><term>DNA Repair</term><term>Disease Models, Animal</term><term>Immunoprecipitation</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Immunoprécipitation</term><term>Immunoprécipitation de la chromatine</term><term>Modèles animaux de maladie humaine</term><term>Réparation de l'ADN</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Technique de Western</term><term>Test des comètes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxygen is supplied as a supportive treatment for patients suffering from acute respiratory distress syndrome. Unfortunately, high oxygen concentration increases reactive oxygen species generation, which causes DNA damage and ultimately cell death in the lung. Although 8-oxoguanine-DNA glycosylase (OGG-1) is involved in repairing hyperoxia-mediated DNA damage, the underlying molecular mechanism remains elusive. In this study, we report that <i>ogg-1</i>-deficient mice exhibited a significant increase of proinflammatory cytokines (TNF-α, IL-6, and IFN-γ) in the lung after being exposed to 95% oxygen. In addition, we found that <i>ogg-1</i> deficiency downregulated (macro)autophagy when exposed to hyperoxia both in vitro and in vivo, which was evident by decreased conversion of LC3-I to LC3-II, reduced LC3 punctate staining, and lower Atg7 expression compared with controls. Using a chromatin immunoprecipitation assay, we found that OGG-1 associated with the promoter of Atg7, suggesting a role for OGG1 in regulation of Atg7 activity. Knocking down OGG-1 decreased the luciferase reporter activity of Atg7. Further, inflammatory cytokine levels in murine lung epithelial cell line cells were downregulated following autophagy induction by starvation and rapamycin treatment, and upregulated when autophagy was blocked using 3-methyladenine and chloroquine. <i>atg7</i> knockout mice and Atg7 small interfering RNA-treated cells exhibited elevated levels of phospho-NF-κB and intensified inflammatory cytokines, suggesting that Atg7 impacts inflammatory responses to hyperoxia. These findings demonstrate that OGG-1 negatively regulates inflammatory cytokine release by coordinating molecular interaction with the autophagic pathway in hyperoxia-induced lung injury.</div></front></TEI><affiliations><list><country><li>Japon</li><li>États-Unis</li></country><region><li>Connecticut</li><li>Dakota du Nord</li></region></list><tree><country name="États-Unis"><region name="Dakota du Nord"><name sortKey="Ye, Yan" sort="Ye, Yan" uniqKey="Ye Y" first="Yan" last="Ye">Yan Ye</name></region><name sortKey="Dhasarathy, Archana" sort="Dhasarathy, Archana" uniqKey="Dhasarathy A" first="Archana" last="Dhasarathy">Archana Dhasarathy</name><name sortKey="Koff, Jonathan L" sort="Koff, Jonathan L" uniqKey="Koff J" first="Jonathan L" last="Koff">Jonathan L. Koff</name><name sortKey="Li, Rongpeng" sort="Li, Rongpeng" uniqKey="Li R" first="Rongpeng" last="Li">Rongpeng Li</name><name sortKey="Lin, Ping" sort="Lin, Ping" uniqKey="Lin P" first="Ping" last="Lin">Ping Lin</name><name sortKey="Pu, Qinqin" sort="Pu, Qinqin" uniqKey="Pu Q" first="Qinqin" last="Pu">Qinqin Pu</name><name sortKey="Tan, Shirui" sort="Tan, Shirui" uniqKey="Tan S" first="Shirui" last="Tan">Shirui Tan</name><name sortKey="Zhang, Weidong" sort="Zhang, Weidong" uniqKey="Zhang W" first="Weidong" last="Zhang">Weidong Zhang</name><name sortKey="Zhou, Xikun" sort="Zhou, Xikun" uniqKey="Zhou X" first="Xikun" last="Zhou">Xikun Zhou</name></country><country name="Japon"><noRegion><name sortKey="Ma, Feng" sort="Ma, Feng" uniqKey="Ma F" first="Feng" last="Ma">Feng Ma</name></noRegion><name sortKey="Deng, Xin" sort="Deng, Xin" uniqKey="Deng X" first="Xin" last="Deng">Xin Deng</name><name sortKey="Jiang, Jianxin" sort="Jiang, Jianxin" uniqKey="Jiang J" first="Jianxin" last="Jiang">Jianxin Jiang</name><name sortKey="Wu, Min" sort="Wu, Min" uniqKey="Wu M" first="Min" last="Wu">Min Wu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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