Cigarette smoke-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages.
Identifieur interne : 000012 ( PubMed/Checkpoint ); précédent : 000011; suivant : 000013Cigarette smoke-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages.
Auteurs : Yanqing Le [République populaire de Chine] ; Yanhong Wang [République populaire de Chine] ; Lu Zhou [République populaire de Chine] ; Jing Xiong [République populaire de Chine] ; Jieyu Tian [République populaire de Chine] ; Xia Yang [République populaire de Chine] ; Xiaoyan Gai [République populaire de Chine] ; Yongchang Sun [République populaire de Chine]Source :
- Journal of cellular and molecular medicine [ 1582-4934 ] ; 2020.
Abstract
High-mobility group box 1 (HMGB1) shows pro-inflammatory activity in various inflammatory diseases and has been found up-regulated in chronic obstructive pulmonary disease (COPD). Lung macrophages play an important role in airway inflammation and lung destruction in COPD, yet whether HMGB1 is involved in cigarette smoke (CS)-induced lung macrophage dysfunction is unknown. We sought to evaluate the intracellular localization and release of HMGB1 in lung macrophages from COPD patients and CS-exposed mice, and to investigate the role of HMGB1 in regulating autophagy in CS extract (CSE)-treated lung macrophages (MH-S cells). Our results showed that HMGB1 was highly expressed in lung tissues and sera of COPD patients and CS-exposed mice, along with predominantly cytoplasmic exporting from nuclei in lung macrophages. In vitro experiments revealed that CSE promoted the expression, nucleocytoplasmic translocation and release of HMGB1 partly via the nicotinic acetylcholine receptor (nAChR). Blockade of HMGB1 with chicken anti-HMGB1 polyclonal antibody (anti-HMGB1) or glycyrrhizin (Gly) attenuated the increase of LC3B-II and Beclin1, migration and p65 phosphorylation, suggesting the involvement of HMGB1 in autophagy, migration and NF-κB activation of lung macrophages. Hydroxychloroquine (CQ), an autophagy inhibitor, enhanced the increase of LC3B-II but not Beclin1 in CSE or rHMGB1-treated MH-S cells, and inhibition of autophagy by CQ and 3-methyladenine (3-MA) abrogated the migration and p65 phosphorylation of CSE-treated cells. These results indicate that CS-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages, providing novel evidence for HMGB1 as a potential target of intervention in COPD.
DOI: 10.1111/jcmm.14789
PubMed: 31769590
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Chine</country><wicri:regionArea>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Wang, Yanhong" sort="Wang, Yanhong" uniqKey="Wang Y" first="Yanhong" last="Wang">Yanhong Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Zhongshan City People's Hospital, Zhongshan, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Zhongshan City People's Hospital, Zhongshan</wicri:regionArea><wicri:noRegion>Zhongshan</wicri:noRegion></affiliation></author><author><name sortKey="Zhou, Lu" sort="Zhou, Lu" uniqKey="Zhou L" first="Lu" last="Zhou">Lu Zhou</name><affiliation wicri:level="3"><nlm:affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Xiong, Jing" sort="Xiong, Jing" uniqKey="Xiong J" first="Jing" last="Xiong">Jing Xiong</name><affiliation wicri:level="3"><nlm:affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Tian, Jieyu" sort="Tian, Jieyu" uniqKey="Tian J" first="Jieyu" last="Tian">Jieyu Tian</name><affiliation wicri:level="3"><nlm:affiliation>Hematology Oncology Center, Beijing Children's Hospital, Capital Medical University, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Hematology Oncology Center, Beijing Children's Hospital, Capital Medical University, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Yang, Xia" sort="Yang, Xia" uniqKey="Yang X" first="Xia" last="Yang">Xia Yang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Tianjin Medical University General Hospital, Tianjing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Tianjin Medical University General Hospital, Tianjing</wicri:regionArea><wicri:noRegion>Tianjing</wicri:noRegion></affiliation></author><author><name sortKey="Gai, Xiaoyan" sort="Gai, Xiaoyan" uniqKey="Gai X" first="Xiaoyan" last="Gai">Xiaoyan Gai</name><affiliation wicri:level="3"><nlm:affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Sun, Yongchang" sort="Sun, Yongchang" uniqKey="Sun Y" first="Yongchang" last="Sun">Yongchang Sun</name><affiliation wicri:level="3"><nlm:affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">Journal of cellular and molecular medicine</title><idno type="eISSN">1582-4934</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">High-mobility group box 1 (HMGB1) shows pro-inflammatory activity in various inflammatory diseases and has been found up-regulated in chronic obstructive pulmonary disease (COPD). Lung macrophages play an important role in airway inflammation and lung destruction in COPD, yet whether HMGB1 is involved in cigarette smoke (CS)-induced lung macrophage dysfunction is unknown. We sought to evaluate the intracellular localization and release of HMGB1 in lung macrophages from COPD patients and CS-exposed mice, and to investigate the role of HMGB1 in regulating autophagy in CS extract (CSE)-treated lung macrophages (MH-S cells). Our results showed that HMGB1 was highly expressed in lung tissues and sera of COPD patients and CS-exposed mice, along with predominantly cytoplasmic exporting from nuclei in lung macrophages. In vitro experiments revealed that CSE promoted the expression, nucleocytoplasmic translocation and release of HMGB1 partly via the nicotinic acetylcholine receptor (nAChR). Blockade of HMGB1 with chicken anti-HMGB1 polyclonal antibody (anti-HMGB1) or glycyrrhizin (Gly) attenuated the increase of LC3B-II and Beclin1, migration and p65 phosphorylation, suggesting the involvement of HMGB1 in autophagy, migration and NF-κB activation of lung macrophages. Hydroxychloroquine (CQ), an autophagy inhibitor, enhanced the increase of LC3B-II but not Beclin1 in CSE or rHMGB1-treated MH-S cells, and inhibition of autophagy by CQ and 3-methyladenine (3-MA) abrogated the migration and p65 phosphorylation of CSE-treated cells. These results indicate that CS-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages, providing novel evidence for HMGB1 as a potential target of intervention in COPD.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">31769590</PMID><DateRevised><Year>2020</Year><Month>02</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1582-4934</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>2</Issue><PubDate><Year>2020</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of cellular and molecular medicine</Title><ISOAbbreviation>J. Cell. Mol. Med.</ISOAbbreviation></Journal><ArticleTitle>Cigarette smoke-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages.</ArticleTitle><Pagination><MedlinePgn>1319-1331</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jcmm.14789</ELocationID><Abstract><AbstractText>High-mobility group box 1 (HMGB1) shows pro-inflammatory activity in various inflammatory diseases and has been found up-regulated in chronic obstructive pulmonary disease (COPD). Lung macrophages play an important role in airway inflammation and lung destruction in COPD, yet whether HMGB1 is involved in cigarette smoke (CS)-induced lung macrophage dysfunction is unknown. We sought to evaluate the intracellular localization and release of HMGB1 in lung macrophages from COPD patients and CS-exposed mice, and to investigate the role of HMGB1 in regulating autophagy in CS extract (CSE)-treated lung macrophages (MH-S cells). Our results showed that HMGB1 was highly expressed in lung tissues and sera of COPD patients and CS-exposed mice, along with predominantly cytoplasmic exporting from nuclei in lung macrophages. In vitro experiments revealed that CSE promoted the expression, nucleocytoplasmic translocation and release of HMGB1 partly via the nicotinic acetylcholine receptor (nAChR). Blockade of HMGB1 with chicken anti-HMGB1 polyclonal antibody (anti-HMGB1) or glycyrrhizin (Gly) attenuated the increase of LC3B-II and Beclin1, migration and p65 phosphorylation, suggesting the involvement of HMGB1 in autophagy, migration and NF-κB activation of lung macrophages. Hydroxychloroquine (CQ), an autophagy inhibitor, enhanced the increase of LC3B-II but not Beclin1 in CSE or rHMGB1-treated MH-S cells, and inhibition of autophagy by CQ and 3-methyladenine (3-MA) abrogated the migration and p65 phosphorylation of CSE-treated cells. These results indicate that CS-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages, providing novel evidence for HMGB1 as a potential target of intervention in COPD.</AbstractText><CopyrightInformation>© 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Le</LastName><ForeName>Yanqing</ForeName><Initials>Y</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-3635-2724</Identifier><AffiliationInfo><Affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yanhong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Zhongshan City People's Hospital, Zhongshan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Lu</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiong</LastName><ForeName>Jing</ForeName><Initials>J</Initials><Identifier Source="ORCID">https://orcid.org/0000-0001-7397-1893</Identifier><AffiliationInfo><Affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tian</LastName><ForeName>Jieyu</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Hematology Oncology Center, Beijing Children's Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xia</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Tianjin Medical University General Hospital, Tianjing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gai</LastName><ForeName>Xiaoyan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Yongchang</ForeName><Initials>Y</Initials><Identifier Source="ORCID">https://orcid.org/0000-0003-3281-8854</Identifier><AffiliationInfo><Affiliation>Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>7192224</GrantID><Agency>Natural Science Foundation of Beijing Municipality</Agency><Country></Country></Grant><Grant><GrantID>81770040</GrantID><Agency>National Natural Science Foundation of China</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>11</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Cell Mol Med</MedlineTA><NlmUniqueID>101083777</NlmUniqueID><ISSNLinking>1582-1838</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">chronic obstructive pulmonary disease</Keyword><Keyword MajorTopicYN="N">high-mobility group box 1</Keyword><Keyword MajorTopicYN="N">lung macrophage</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>05</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>09</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>10</Month><Day>04</Day></PubMedPubDate><PubMedPubDate 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sort="Gai, Xiaoyan" uniqKey="Gai X" first="Xiaoyan" last="Gai">Xiaoyan Gai</name><name sortKey="Sun, Yongchang" sort="Sun, Yongchang" uniqKey="Sun Y" first="Yongchang" last="Sun">Yongchang Sun</name><name sortKey="Tian, Jieyu" sort="Tian, Jieyu" uniqKey="Tian J" first="Jieyu" last="Tian">Jieyu Tian</name><name sortKey="Wang, Yanhong" sort="Wang, Yanhong" uniqKey="Wang Y" first="Yanhong" last="Wang">Yanhong Wang</name><name sortKey="Xiong, Jing" sort="Xiong, Jing" uniqKey="Xiong J" first="Jing" last="Xiong">Jing Xiong</name><name sortKey="Yang, Xia" sort="Yang, Xia" uniqKey="Yang X" first="Xia" last="Yang">Xia Yang</name><name sortKey="Zhou, Lu" sort="Zhou, Lu" uniqKey="Zhou L" first="Lu" last="Zhou">Lu Zhou</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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