Autophagy protects against ischemia/reperfusion-induced lung injury through alleviating blood-air barrier damage.
Identifieur interne : 000255 ( PubMed/Curation ); précédent : 000254; suivant : 000256Autophagy protects against ischemia/reperfusion-induced lung injury through alleviating blood-air barrier damage.
Auteurs : Dan Zhang [République populaire de Chine] ; Chichi Li [République populaire de Chine] ; Jian Zhou [République populaire de Chine] ; Yuanlin Song [République populaire de Chine] ; Xiaocong Fang [République populaire de Chine] ; Jiaxian Ou [République populaire de Chine] ; Jing Li [République populaire de Chine] ; Chunxue Bai [République populaire de Chine]Source :
- The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation [ 1557-3117 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Autophagie (physiologie), Barrière alvéolocapillaire (physiologie), Cellules cultivées, Endothélium vasculaire (anatomopathologie), Endothélium vasculaire (métabolisme), Humains, Lésion d'ischémie-reperfusion (anatomopathologie), Lésion d'ischémie-reperfusion (métabolisme), Lésion pulmonaire (anatomopathologie), Lésion pulmonaire (métabolisme), Souris, Survie cellulaire.
- MESH :
- anatomopathologie : Endothélium vasculaire, Lésion d'ischémie-reperfusion, Lésion pulmonaire.
- métabolisme : Endothélium vasculaire, Lésion d'ischémie-reperfusion, Lésion pulmonaire.
- physiologie : Autophagie, Barrière alvéolocapillaire.
- Animaux, Cellules cultivées, Humains, Souris, Survie cellulaire.
English descriptors
- KwdEn :
- MESH :
- metabolism : Endothelium, Vascular, Lung Injury, Reperfusion Injury.
- pathology : Endothelium, Vascular, Lung Injury, Reperfusion Injury.
- physiology : Autophagy, Blood-Air Barrier.
- Animals, Cell Survival, Cells, Cultured, Humans, Mice.
Abstract
Understanding the role and underlying regulation mechanism of autophagy in ischemia/reperfusion (I/R)-induced lung injury may provide potentially new pharmacologic targets for treatment of acute lung injury. The aim of this study was to adjust autophagy with pharmacologic agents to determine its functional significance in I/R-induced lung injury.
DOI: 10.1016/j.healun.2014.12.008
PubMed: 25934479
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Electronic address: cxbai@fudan.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai</wicri:regionArea></affiliation></author></analytic><series><title level="j">The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation</title><idno type="eISSN">1557-3117</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autophagy (physiology)</term><term>Blood-Air Barrier (physiology)</term><term>Cell Survival</term><term>Cells, Cultured</term><term>Endothelium, Vascular (metabolism)</term><term>Endothelium, Vascular (pathology)</term><term>Humans</term><term>Lung Injury (metabolism)</term><term>Lung Injury (pathology)</term><term>Mice</term><term>Reperfusion Injury (metabolism)</term><term>Reperfusion Injury (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Autophagie (physiologie)</term><term>Barrière alvéolocapillaire (physiologie)</term><term>Cellules cultivées</term><term>Endothélium vasculaire (anatomopathologie)</term><term>Endothélium vasculaire (métabolisme)</term><term>Humains</term><term>Lésion d'ischémie-reperfusion (anatomopathologie)</term><term>Lésion d'ischémie-reperfusion (métabolisme)</term><term>Lésion pulmonaire (anatomopathologie)</term><term>Lésion pulmonaire (métabolisme)</term><term>Souris</term><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Endothélium vasculaire</term><term>Lésion d'ischémie-reperfusion</term><term>Lésion pulmonaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelium, Vascular</term><term>Lung Injury</term><term>Reperfusion Injury</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Endothélium vasculaire</term><term>Lésion d'ischémie-reperfusion</term><term>Lésion pulmonaire</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endothelium, Vascular</term><term>Lung Injury</term><term>Reperfusion Injury</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Autophagie</term><term>Barrière alvéolocapillaire</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term><term>Blood-Air Barrier</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Survival</term><term>Cells, Cultured</term><term>Humans</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Humains</term><term>Souris</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Understanding the role and underlying regulation mechanism of autophagy in ischemia/reperfusion (I/R)-induced lung injury may provide potentially new pharmacologic targets for treatment of acute lung injury. The aim of this study was to adjust autophagy with pharmacologic agents to determine its functional significance in I/R-induced lung injury.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25934479</PMID><DateCompleted><Year>2016</Year><Month>01</Month><Day>26</Day></DateCompleted><DateRevised><Year>2015</Year><Month>05</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-3117</ISSN><JournalIssue CitedMedium="Internet"><Volume>34</Volume><Issue>5</Issue><PubDate><Year>2015</Year><Month>May</Month></PubDate></JournalIssue><Title>The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation</Title><ISOAbbreviation>J. Heart Lung Transplant.</ISOAbbreviation></Journal><ArticleTitle>Autophagy protects against ischemia/reperfusion-induced lung injury through alleviating blood-air barrier damage.</ArticleTitle><Pagination><MedlinePgn>746-55</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.healun.2014.12.008</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1053-2498(14)01503-4</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Understanding the role and underlying regulation mechanism of autophagy in ischemia/reperfusion (I/R)-induced lung injury may provide potentially new pharmacologic targets for treatment of acute lung injury. The aim of this study was to adjust autophagy with pharmacologic agents to determine its functional significance in I/R-induced lung injury.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Human pulmonary microvascular endothelial cells (HPMVECs) and mice were pre-conditioned with autophagy inhibitor chloroquine or promoter rapamycin before they were challenged with oxygen-glucose deprivation/oxygen-glucose restoration (OGD) and lung I/R, respectively. Extracellular signal-regulated kinase (ERK)1/2 inhibitor U0126 was pre-injected into I/R-induced mice to test the role of ERK1/2 in regulating autophagy.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">OGD caused tight conjunction damage and cell death in HPMVECs, which was further aggravated by blocking autophagy, yet ameliorated through promoting autophagy. On a consistent basis, inhibiting autophagy aggravated I/R-induced lung edema and tissue inflammation, which was significantly alleviated by promoting autophagy with rapamycin. In addition, inhibition of ERK1/2 increased expression of active mammalian target-of-rapamycin and thus decreased I/R-induced autophagy.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">It appears that autophagy plays a protective role in I/R-induced lung injury and this effect may be enhanced by moderately improving autophagy level. Meanwhile, the ERK1/2 signal pathway has a positively regulating role in lung I/R-induced autophagy.</AbstractText><CopyrightInformation>Copyright © 2015 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Dan</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Chichi</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou city, Zhejiang Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Jian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Yuanlin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Xiaocong</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ou</LastName><ForeName>Jiaxian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Chunxue</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address: cxbai@fudan.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>12</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Heart Lung Transplant</MedlineTA><NlmUniqueID>9102703</NlmUniqueID><ISSNLinking>1053-2498</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015824" MajorTopicYN="N">Blood-Air Barrier</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004730" MajorTopicYN="N">Endothelium, Vascular</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055370" MajorTopicYN="N">Lung Injury</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015427" MajorTopicYN="N">Reperfusion Injury</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">acute lung injury</Keyword><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">extracellular signal-regulated kinase</Keyword><Keyword MajorTopicYN="N">ischemia/reperfusion</Keyword><Keyword MajorTopicYN="N">rapamycin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>02</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>11</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>12</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>5</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>5</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>1</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25934479</ArticleId><ArticleId IdType="pii">S1053-2498(14)01503-4</ArticleId><ArticleId IdType="doi">10.1016/j.healun.2014.12.008</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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