Integrin αvβ5 inhibition protects against ischemia-reperfusion-induced lung injury in an autophagy-dependent manner.
Identifieur interne : 000161 ( PubMed/Corpus ); précédent : 000160; suivant : 000162Integrin αvβ5 inhibition protects against ischemia-reperfusion-induced lung injury in an autophagy-dependent manner.
Auteurs : Dan Zhang ; Chichi Li ; Yuanlin Song ; Jian Zhou ; Yuping Li ; Jing Li ; Chunxue BaiSource :
- American journal of physiology. Lung cellular and molecular physiology [ 1522-1504 ] ; 2017.
English descriptors
- KwdEn :
- Acute Lung Injury (drug therapy), Acute Lung Injury (metabolism), Animals, Apoptosis (drug effects), Autophagy (drug effects), Bronchoalveolar Lavage Fluid (chemistry), Caspase 3 (metabolism), Cells, Cultured, Endothelial Cells (drug effects), Endothelial Cells (metabolism), Glucose (metabolism), Humans, Lung (drug effects), Lung (metabolism), Mice, Mice, Inbred C57BL, Oxygen (metabolism), Protective Agents (pharmacology), Receptors, Vitronectin (antagonists & inhibitors), Receptors, Vitronectin (metabolism), Reperfusion Injury (drug therapy), Reperfusion Injury (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Receptors, Vitronectin.
- chemical , metabolism : Caspase 3, Glucose, Oxygen, Receptors, Vitronectin.
- chemistry : Bronchoalveolar Lavage Fluid.
- drug effects : Apoptosis, Autophagy, Endothelial Cells, Lung.
- drug therapy : Acute Lung Injury, Reperfusion Injury.
- metabolism : Acute Lung Injury, Endothelial Cells, Lung, Reperfusion Injury.
- chemical , pharmacology : Protective Agents.
- Animals, Cells, Cultured, Humans, Mice, Mice, Inbred C57BL.
Abstract
Integrin αvβ5 mediates pulmonary endothelial barrier function and acute lung injury (LI), but its roles in cell apoptosis and autophagy are unclear. Thus, the aims of this study were to investigate the significance of αvβ5 in ischemia-reperfusion (I/R)-induced apoptosis and LI and to explore the relationship between αvβ5 and autophagy. Human pulmonary microvascular endothelial cells (HPMVECs) were pretreated with an αvβ5-blocking antibody (ALULA) and challenged with oxygen-glucose deprivation/oxygen-glucose restoration, which mimics I/R; then, cellular autophagy and apoptosis were detected, and cell permeability was assessed. In vivo, mice were pretreated with the autophagy inhibitor chloroquine (CLQ), followed by treatment with ALULA. The mice then underwent operative lung I/R. LI was assessed by performing a pathological examination, calculating the wet/dry lung weight ratio and detecting the bronchial alveolar lavage fluid (BALF) protein concentration. αvβ5 inhibition promoted HPMVEC autophagy under I/R in vitro, alleviated cell permeability, decreased the apoptosis ratio, and activated caspase-3 expression. These outcomes were significantly diminished when autophagy was inhibited with a small-interfering RNA construct targeting autophagy-related gene 7 (siATG7). Moreover, ALULA pretreatment alleviated I/R-induced LI (I/R-LI), which manifested as a decreased wet/dry lung weight ratio, an altered BALF protein concentration, and lung edema. Preinhibiting autophagy with CLQ, however, eliminated the protective effects of ALULA on I/R-LI. Therefore, inhibiting αvβ5 effectively ameliorated I/R-induced endothelial cell apoptosis and I/R-LI. This process was dependent on improved autophagy and its inhibitory effects on activated caspase-3.
DOI: 10.1152/ajplung.00391.2016
PubMed: 28522565
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pubmed:28522565Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Integrin αvβ5 inhibition protects against ischemia-reperfusion-induced lung injury in an autophagy-dependent manner.</title><author><name sortKey="Zhang, Dan" sort="Zhang, Dan" uniqKey="Zhang D" first="Dan" last="Zhang">Dan Zhang</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Chichi" sort="Li, Chichi" uniqKey="Li C" first="Chichi" last="Li">Chichi Li</name><affiliation><nlm:affiliation>Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation></affiliation></author><author><name sortKey="Song, Yuanlin" sort="Song, Yuanlin" uniqKey="Song Y" first="Yuanlin" last="Song">Yuanlin Song</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Yuping" sort="Li, Yuping" uniqKey="Li Y" first="Yuping" last="Li">Yuping Li</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Jing" sort="Li, Jing" uniqKey="Li J" first="Jing" last="Li">Jing Li</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Bai, Chunxue" sort="Bai, Chunxue" uniqKey="Bai C" first="Chunxue" last="Bai">Chunxue Bai</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China; cxbai@fudan.edu.cn.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28522565</idno><idno type="pmid">28522565</idno><idno type="doi">10.1152/ajplung.00391.2016</idno><idno type="wicri:Area/PubMed/Corpus">000161</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000161</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Integrin αvβ5 inhibition protects against ischemia-reperfusion-induced lung injury in an autophagy-dependent manner.</title><author><name sortKey="Zhang, Dan" sort="Zhang, Dan" uniqKey="Zhang D" first="Dan" last="Zhang">Dan Zhang</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Chichi" sort="Li, Chichi" uniqKey="Li C" first="Chichi" last="Li">Chichi Li</name><affiliation><nlm:affiliation>Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation></affiliation></author><author><name sortKey="Song, Yuanlin" sort="Song, Yuanlin" uniqKey="Song Y" first="Yuanlin" last="Song">Yuanlin Song</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Yuping" sort="Li, Yuping" uniqKey="Li Y" first="Yuping" last="Li">Yuping Li</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Jing" sort="Li, Jing" uniqKey="Li J" first="Jing" last="Li">Jing Li</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Bai, Chunxue" sort="Bai, Chunxue" uniqKey="Bai C" first="Chunxue" last="Bai">Chunxue Bai</name><affiliation><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China; cxbai@fudan.edu.cn.</nlm:affiliation></affiliation></author></analytic><series><title level="j">American journal of physiology. Lung cellular and molecular physiology</title><idno type="eISSN">1522-1504</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 (drug therapy)</term><term>Acute Lung Injury (metabolism)</term><term>Animals</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Bronchoalveolar Lavage Fluid (chemistry)</term><term>Caspase 3 (metabolism)</term><term>Cells, Cultured</term><term>Endothelial Cells (drug effects)</term><term>Endothelial Cells (metabolism)</term><term>Glucose (metabolism)</term><term>Humans</term><term>Lung (drug effects)</term><term>Lung (metabolism)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Oxygen (metabolism)</term><term>Protective Agents (pharmacology)</term><term>Receptors, Vitronectin (antagonists & inhibitors)</term><term>Receptors, Vitronectin (metabolism)</term><term>Reperfusion Injury (drug therapy)</term><term>Reperfusion Injury (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, Vitronectin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 3</term><term>Glucose</term><term>Oxygen</term><term>Receptors, Vitronectin</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Bronchoalveolar Lavage Fluid</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Endothelial Cells</term><term>Lung</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Acute Lung Injury</term><term>Reperfusion Injury</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Acute Lung Injury</term><term>Endothelial Cells</term><term>Lung</term><term>Reperfusion Injury</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Protective Agents</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Integrin αvβ5 mediates pulmonary endothelial barrier function and acute lung injury (LI), but its roles in cell apoptosis and autophagy are unclear. Thus, the aims of this study were to investigate the significance of αvβ5 in ischemia-reperfusion (I/R)-induced apoptosis and LI and to explore the relationship between αvβ5 and autophagy. Human pulmonary microvascular endothelial cells (HPMVECs) were pretreated with an αvβ5-blocking antibody (ALULA) and challenged with oxygen-glucose deprivation/oxygen-glucose restoration, which mimics I/R; then, cellular autophagy and apoptosis were detected, and cell permeability was assessed. In vivo, mice were pretreated with the autophagy inhibitor chloroquine (CLQ), followed by treatment with ALULA. The mice then underwent operative lung I/R. LI was assessed by performing a pathological examination, calculating the wet/dry lung weight ratio and detecting the bronchial alveolar lavage fluid (BALF) protein concentration. αvβ5 inhibition promoted HPMVEC autophagy under I/R in vitro, alleviated cell permeability, decreased the apoptosis ratio, and activated caspase-3 expression. These outcomes were significantly diminished when autophagy was inhibited with a small-interfering RNA construct targeting autophagy-related gene 7 (si<i>ATG</i>7). Moreover, ALULA pretreatment alleviated I/R-induced LI (I/R-LI), which manifested as a decreased wet/dry lung weight ratio, an altered BALF protein concentration, and lung edema. Preinhibiting autophagy with CLQ, however, eliminated the protective effects of ALULA on I/R-LI. Therefore, inhibiting αvβ5 effectively ameliorated I/R-induced endothelial cell apoptosis and I/R-LI. This process was dependent on improved autophagy and its inhibitory effects on activated caspase-3.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28522565</PMID><DateCompleted><Year>2017</Year><Month>08</Month><Day>29</Day></DateCompleted><DateRevised><Year>2018</Year><Month>06</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1504</ISSN><JournalIssue CitedMedium="Internet"><Volume>313</Volume><Issue>2</Issue><PubDate><Year>2017</Year><Month>08</Month><Day>01</Day></PubDate></JournalIssue><Title>American journal of physiology. Lung cellular and molecular physiology</Title><ISOAbbreviation>Am. J. Physiol. Lung Cell Mol. Physiol.</ISOAbbreviation></Journal><ArticleTitle>Integrin αvβ5 inhibition protects against ischemia-reperfusion-induced lung injury in an autophagy-dependent manner.</ArticleTitle><Pagination><MedlinePgn>L384-L394</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajplung.00391.2016</ELocationID><Abstract><AbstractText>Integrin αvβ5 mediates pulmonary endothelial barrier function and acute lung injury (LI), but its roles in cell apoptosis and autophagy are unclear. Thus, the aims of this study were to investigate the significance of αvβ5 in ischemia-reperfusion (I/R)-induced apoptosis and LI and to explore the relationship between αvβ5 and autophagy. Human pulmonary microvascular endothelial cells (HPMVECs) were pretreated with an αvβ5-blocking antibody (ALULA) and challenged with oxygen-glucose deprivation/oxygen-glucose restoration, which mimics I/R; then, cellular autophagy and apoptosis were detected, and cell permeability was assessed. In vivo, mice were pretreated with the autophagy inhibitor chloroquine (CLQ), followed by treatment with ALULA. The mice then underwent operative lung I/R. LI was assessed by performing a pathological examination, calculating the wet/dry lung weight ratio and detecting the bronchial alveolar lavage fluid (BALF) protein concentration. αvβ5 inhibition promoted HPMVEC autophagy under I/R in vitro, alleviated cell permeability, decreased the apoptosis ratio, and activated caspase-3 expression. These outcomes were significantly diminished when autophagy was inhibited with a small-interfering RNA construct targeting autophagy-related gene 7 (si<i>ATG</i>7). Moreover, ALULA pretreatment alleviated I/R-induced LI (I/R-LI), which manifested as a decreased wet/dry lung weight ratio, an altered BALF protein concentration, and lung edema. Preinhibiting autophagy with CLQ, however, eliminated the protective effects of ALULA on I/R-LI. Therefore, inhibiting αvβ5 effectively ameliorated I/R-induced endothelial cell apoptosis and I/R-LI. This process was dependent on improved autophagy and its inhibitory effects on activated caspase-3.</AbstractText><CopyrightInformation>Copyright © 2017 the American Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Dan</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, 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, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Yuanlin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Jian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yuping</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Chunxue</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China; cxbai@fudan.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China; and.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong Province, China.</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>2017</Year><Month>05</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Lung Cell Mol Physiol</MedlineTA><NlmUniqueID>100901229</NlmUniqueID><ISSNLinking>1040-0605</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020011">Protective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019030">Receptors, Vitronectin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C064660">integrin alphaVbeta5</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053148">Caspase 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>S88TT14065</RegistryNumber><NameOfSubstance UI="D010100">Oxygen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D055371" MajorTopicYN="N">Acute Lung Injury</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001992" MajorTopicYN="N">Bronchoalveolar Lavage Fluid</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053148" MajorTopicYN="N">Caspase 3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010100" MajorTopicYN="N">Oxygen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020011" MajorTopicYN="N">Protective Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019030" MajorTopicYN="N">Receptors, Vitronectin</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015427" MajorTopicYN="N">Reperfusion Injury</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">apoptosis</Keyword><Keyword MajorTopicYN="Y">autophagy</Keyword><Keyword MajorTopicYN="Y">integrin αvβ5</Keyword><Keyword MajorTopicYN="Y">lung injury</Keyword><Keyword MajorTopicYN="Y">lung ischemia-reperfusion</Keyword><Keyword MajorTopicYN="Y">oxygen-glucose deprivation/oxygen-glucose restoration</Keyword><Keyword MajorTopicYN="Y">pulmonary microvascular endothelial cells</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>09</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>04</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>05</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>5</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>8</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>5</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28522565</ArticleId><ArticleId IdType="pii">ajplung.00391.2016</ArticleId><ArticleId 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