DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.
Identifieur interne : 000176 ( PubMed/Corpus ); précédent : 000175; suivant : 000177DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.
Auteurs : Yan Ye ; Ping Lin ; Weidong Zhang ; Shirui Tan ; Xikun Zhou ; Rongpeng Li ; Qinqin Pu ; Jonathan L. Koff ; Archana Dhasarathy ; Feng Ma ; Xin Deng ; Jianxin Jiang ; Min WuSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2017.
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
Links to Exploration step
pubmed:28202616Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.</title><author><name sortKey="Ye, Yan" sort="Ye, Yan" uniqKey="Ye Y" first="Yan" last="Ye">Yan Ye</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Lin, Ping" sort="Lin, Ping" uniqKey="Lin P" first="Ping" last="Lin">Ping Lin</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Weidong" sort="Zhang, Weidong" uniqKey="Zhang W" first="Weidong" last="Zhang">Weidong Zhang</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Tan, Shirui" sort="Tan, Shirui" uniqKey="Tan S" first="Shirui" last="Tan">Shirui Tan</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Zhou, Xikun" sort="Zhou, Xikun" uniqKey="Zhou X" first="Xikun" last="Zhou">Xikun Zhou</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Rongpeng" sort="Li, Rongpeng" uniqKey="Li R" first="Rongpeng" last="Li">Rongpeng Li</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Pu, Qinqin" sort="Pu, Qinqin" uniqKey="Pu Q" first="Qinqin" last="Pu">Qinqin Pu</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></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><nlm:affiliation>Department of Medicine, Yale University, New Haven, CT 06510.</nlm:affiliation></affiliation></author><author><name sortKey="Dhasarathy, Archana" sort="Dhasarathy, Archana" uniqKey="Dhasarathy A" first="Archana" last="Dhasarathy">Archana Dhasarathy</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Ma, Feng" sort="Ma, Feng" uniqKey="Ma F" first="Feng" last="Ma">Feng Ma</name><affiliation><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></affiliation></author><author><name sortKey="Deng, Xin" sort="Deng, Xin" uniqKey="Deng X" first="Xin" last="Deng">Xin Deng</name><affiliation><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></affiliation></author><author><name sortKey="Jiang, Jianxin" sort="Jiang, Jianxin" uniqKey="Jiang J" first="Jianxin" last="Jiang">Jianxin Jiang</name><affiliation><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></affiliation></author><author><name sortKey="Wu, Min" sort="Wu, Min" uniqKey="Wu M" first="Min" last="Wu">Min Wu</name><affiliation><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></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28202616</idno><idno type="pmid">28202616</idno><idno type="doi">10.4049/jimmunol.1601001</idno><idno type="wicri:Area/PubMed/Corpus">000176</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000176</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.</title><author><name sortKey="Ye, Yan" sort="Ye, Yan" uniqKey="Ye Y" first="Yan" last="Ye">Yan Ye</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Lin, Ping" sort="Lin, Ping" uniqKey="Lin P" first="Ping" last="Lin">Ping Lin</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Weidong" sort="Zhang, Weidong" uniqKey="Zhang W" first="Weidong" last="Zhang">Weidong Zhang</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Tan, Shirui" sort="Tan, Shirui" uniqKey="Tan S" first="Shirui" last="Tan">Shirui Tan</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Zhou, Xikun" sort="Zhou, Xikun" uniqKey="Zhou X" first="Xikun" last="Zhou">Xikun Zhou</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Rongpeng" sort="Li, Rongpeng" uniqKey="Li R" first="Rongpeng" last="Li">Rongpeng Li</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Pu, Qinqin" sort="Pu, Qinqin" uniqKey="Pu Q" first="Qinqin" last="Pu">Qinqin Pu</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></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><nlm:affiliation>Department of Medicine, Yale University, New Haven, CT 06510.</nlm:affiliation></affiliation></author><author><name sortKey="Dhasarathy, Archana" sort="Dhasarathy, Archana" uniqKey="Dhasarathy A" first="Archana" last="Dhasarathy">Archana Dhasarathy</name><affiliation><nlm:affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</nlm:affiliation></affiliation></author><author><name sortKey="Ma, Feng" sort="Ma, Feng" uniqKey="Ma F" first="Feng" last="Ma">Feng Ma</name><affiliation><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></affiliation></author><author><name sortKey="Deng, Xin" sort="Deng, Xin" uniqKey="Deng X" first="Xin" last="Deng">Xin Deng</name><affiliation><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></affiliation></author><author><name sortKey="Jiang, Jianxin" sort="Jiang, Jianxin" uniqKey="Jiang J" first="Jianxin" last="Jiang">Jianxin Jiang</name><affiliation><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></affiliation></author><author><name sortKey="Wu, Min" sort="Wu, Min" uniqKey="Wu M" first="Min" last="Wu">Min Wu</name><affiliation><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></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="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><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="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></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28202616</PMID><DateCompleted><Year>2017</Year><Month>08</Month><Day>15</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>198</Volume><Issue>7</Issue><PubDate><Year>2017</Year><Month>04</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.</ArticleTitle><Pagination><MedlinePgn>2844-2853</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1601001</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>Copyright © 2017 by The American Association of Immunologists, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ye</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Ping</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</Affiliation></AffiliationInfo><AffiliationInfo><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.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Weidong</ForeName><Initials>W</Initials><Identifier Source="ORCID">0000-0003-2941-4285</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Shirui</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-6740-880X</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Xikun</ForeName><Initials>X</Initials><Identifier Source="ORCID">0000-0001-6768-2382</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Rongpeng</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Key Laboratory of Biotechnology for Medicinal Plants of Jiangsu Province, Jiangsu Normal University, Xuzhou, Jiangsu 2211116, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pu</LastName><ForeName>Qinqin</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koff</LastName><ForeName>Jonathan L</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>Department of Medicine, Yale University, New Haven, CT 06510.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dhasarathy</LastName><ForeName>Archana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Feng</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0002-1594-6064</Identifier><AffiliationInfo><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.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><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.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Jianxin</ForeName><Initials>J</Initials><AffiliationInfo><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.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Min</ForeName><Initials>M</Initials><AffiliationInfo><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.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R03 ES014690</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R03 AI097532</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P20 GM113123</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI109317</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL125897</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R15 AI101973</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P20 GM103442</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 GM103329</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.2.2.-</RegistryNumber><NameOfSubstance UI="D045647">DNA Glycosylases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.2.2.-</RegistryNumber><NameOfSubstance UI="C485990">Ogg1 protein, mouse</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>J Immunol. 2017 Jul 15;199(2):381</RefSource><PMID Version="1">28696326</PMID></CommentsCorrections><CommentsCorrections RefType="CommentIn"><RefSource>J Immunol. 2017 Jul 15;199(2):381-382</RefSource><PMID Version="1">28696327</PMID></CommentsCorrections><CommentsCorrections RefType="ErratumIn"><RefSource>J Immunol. 2017 Aug 1;199(3):1207</RefSource><PMID Version="1">28739596</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D055371" MajorTopicYN="N">Acute Lung Injury</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D047369" MajorTopicYN="N">Chromatin Immunoprecipitation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020552" MajorTopicYN="N">Comet Assay</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName 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