Protective effect of autophagy on endoplasmic reticulum stress induced apoptosis of alveolar epithelial cells in rat models of COPD.
Identifieur interne : 000146 ( PubMed/Corpus ); précédent : 000145; suivant : 000147Protective effect of autophagy on endoplasmic reticulum stress induced apoptosis of alveolar epithelial cells in rat models of COPD.
Auteurs : Yao Tang ; Qi-Hang Cai ; Yong-Jian Wang ; Shao-Hua Fan ; Zi-Feng Zhang ; Meng-Qi Xiao ; Jin-Yu Zhu ; Dong-Mei Wu ; Jun Lu ; Yuan-Lin ZhengSource :
- Bioscience reports [ 1573-4935 ] ; 2017.
English descriptors
- KwdEn :
- Adenine (analogs & derivatives), Adenine (pharmacology), Alveolar Epithelial Cells (drug effects), Alveolar Epithelial Cells (pathology), Animals, Apoptosis, Autophagy (drug effects), Biomarkers (metabolism), Chloroquine (pharmacology), Disease Models, Animal, Endoplasmic Reticulum Stress, Male, Pulmonary Disease, Chronic Obstructive (chemically induced), Pulmonary Disease, Chronic Obstructive (pathology), Pulmonary Disease, Chronic Obstructive (physiopathology), Rats, Rats, Sprague-Dawley, Smoke (adverse effects).
- MESH :
- chemical , adverse effects : Smoke.
- chemical , analogs & derivatives : Adenine.
- chemical , metabolism : Biomarkers.
- chemical , pharmacology : Adenine, Chloroquine.
- chemically induced : Pulmonary Disease, Chronic Obstructive.
- drug effects : Alveolar Epithelial Cells, Autophagy.
- pathology : Alveolar Epithelial Cells, Pulmonary Disease, Chronic Obstructive.
- physiopathology : Pulmonary Disease, Chronic Obstructive.
- Animals, Apoptosis, Disease Models, Animal, Endoplasmic Reticulum Stress, Male, Rats, Rats, Sprague-Dawley.
Abstract
During the present study, we explored the protective effects of autophagy on endoplasmic reticulum (ER) stress (ERS) induced apoptosis belonging to alveolar epithelial cells (AECs) in rat models with chronic obstructive pulmonary disease (COPD). Fifty-six 12-week-old male Sprague-Dawley (SD) rats were randomly assigned into the COPD group (rats exposed to cigarette smoke (CS)), the 3-methyladenine (3-MA) intervention group (COPD rats were administrated with 10 mg/kg autophagy inhibitors), the chloroquine (CQ)-intervention group (COPD rats were administrated 40 mg/kg CQ), and the control group (rats breathed in normal saline). The forced expiratory volume in 0.3 s/forced vital capacity (FEV0.3/FVC%), inspiratory resistance (RI), and dynamic lung compliance (Cdyn) were measured and recorded. The expressions of PKR-like ER kinase (PERK) and CCAAT/enhancer-binding protein-homologous protein (CHOP) were detected by immunohistochemistry. The cell apoptotic rates of AECs were analyzed by terminal deoxynucleotidyl transferase (TdT) mediated dUTP-biotin nick end-labeling (TUNEL) staining. The expression levels of light chain 3 (LC3-II), p62, Beclin-1, ATG5, ATG7, Caspase-12, and Caspase-3 were detected by Western blotting. Results showed that the COPD group exhibited a lower FEV0.3/FVC% and Cdyn, and a higher RI than the control group. Compared with the control group, the integrated optical density (IOD) values of PERK and CHOP, the apoptotic rate of AECs, and expressions of LC3-II, Beclin-1, ATG5, ATG7, Caspase-3, and Caspase-12 expressions were significantly higher, whereas p62 expression was significantly lower in the COPD group. Based on the results obtained during the present study, it became clear that the inhibition of autophagy could attenuate the ERS-induced apoptosis of AECs in rats with COPD.
DOI: 10.1042/BSR20170803
PubMed: 28963374
Links to Exploration step
pubmed:28963374Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Protective effect of autophagy on endoplasmic reticulum stress induced apoptosis of alveolar epithelial cells in rat models of COPD.</title><author><name sortKey="Tang, Yao" sort="Tang, Yao" uniqKey="Tang Y" first="Yao" last="Tang">Yao Tang</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Cai, Qi Hang" sort="Cai, Qi Hang" uniqKey="Cai Q" first="Qi-Hang" last="Cai">Qi-Hang Cai</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Yong Jian" sort="Wang, Yong Jian" uniqKey="Wang Y" first="Yong-Jian" last="Wang">Yong-Jian Wang</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Fan, Shao Hua" sort="Fan, Shao Hua" uniqKey="Fan S" first="Shao-Hua" last="Fan">Shao-Hua Fan</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Zi Feng" sort="Zhang, Zi Feng" uniqKey="Zhang Z" first="Zi-Feng" last="Zhang">Zi-Feng Zhang</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Xiao, Meng Qi" sort="Xiao, Meng Qi" uniqKey="Xiao M" first="Meng-Qi" last="Xiao">Meng-Qi Xiao</name><affiliation><nlm:affiliation>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhu, Jin Yu" sort="Zhu, Jin Yu" uniqKey="Zhu J" first="Jin-Yu" last="Zhu">Jin-Yu Zhu</name><affiliation><nlm:affiliation>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Wu, Dong Mei" sort="Wu, Dong Mei" uniqKey="Wu D" first="Dong-Mei" last="Wu">Dong-Mei Wu</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</nlm:affiliation></affiliation></author><author><name sortKey="Lu, Jun" sort="Lu, Jun" uniqKey="Lu J" first="Jun" last="Lu">Jun Lu</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</nlm:affiliation></affiliation></author><author><name sortKey="Zheng, Yuan Lin" sort="Zheng, Yuan Lin" uniqKey="Zheng Y" first="Yuan-Lin" last="Zheng">Yuan-Lin Zheng</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28963374</idno><idno type="pmid">28963374</idno><idno type="doi">10.1042/BSR20170803</idno><idno type="wicri:Area/PubMed/Corpus">000146</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000146</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Protective effect of autophagy on endoplasmic reticulum stress induced apoptosis of alveolar epithelial cells in rat models of COPD.</title><author><name sortKey="Tang, Yao" sort="Tang, Yao" uniqKey="Tang Y" first="Yao" last="Tang">Yao Tang</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Cai, Qi Hang" sort="Cai, Qi Hang" uniqKey="Cai Q" first="Qi-Hang" last="Cai">Qi-Hang Cai</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Yong Jian" sort="Wang, Yong Jian" uniqKey="Wang Y" first="Yong-Jian" last="Wang">Yong-Jian Wang</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Fan, Shao Hua" sort="Fan, Shao Hua" uniqKey="Fan S" first="Shao-Hua" last="Fan">Shao-Hua Fan</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Zi Feng" sort="Zhang, Zi Feng" uniqKey="Zhang Z" first="Zi-Feng" last="Zhang">Zi-Feng Zhang</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Xiao, Meng Qi" sort="Xiao, Meng Qi" uniqKey="Xiao M" first="Meng-Qi" last="Xiao">Meng-Qi Xiao</name><affiliation><nlm:affiliation>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhu, Jin Yu" sort="Zhu, Jin Yu" uniqKey="Zhu J" first="Jin-Yu" last="Zhu">Jin-Yu Zhu</name><affiliation><nlm:affiliation>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Wu, Dong Mei" sort="Wu, Dong Mei" uniqKey="Wu D" first="Dong-Mei" last="Wu">Dong-Mei Wu</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</nlm:affiliation></affiliation></author><author><name sortKey="Lu, Jun" sort="Lu, Jun" uniqKey="Lu J" first="Jun" last="Lu">Jun Lu</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</nlm:affiliation></affiliation></author><author><name sortKey="Zheng, Yuan Lin" sort="Zheng, Yuan Lin" uniqKey="Zheng Y" first="Yuan-Lin" last="Zheng">Yuan-Lin Zheng</name><affiliation><nlm:affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Bioscience reports</title><idno type="eISSN">1573-4935</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenine (analogs & derivatives)</term><term>Adenine (pharmacology)</term><term>Alveolar Epithelial Cells (drug effects)</term><term>Alveolar Epithelial Cells (pathology)</term><term>Animals</term><term>Apoptosis</term><term>Autophagy (drug effects)</term><term>Biomarkers (metabolism)</term><term>Chloroquine (pharmacology)</term><term>Disease Models, Animal</term><term>Endoplasmic Reticulum Stress</term><term>Male</term><term>Pulmonary Disease, Chronic Obstructive (chemically induced)</term><term>Pulmonary Disease, Chronic Obstructive (pathology)</term><term>Pulmonary Disease, Chronic Obstructive (physiopathology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Smoke (adverse effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Smoke</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adenine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenine</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Pulmonary Disease, Chronic Obstructive</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Alveolar Epithelial Cells</term><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alveolar Epithelial Cells</term><term>Pulmonary Disease, Chronic Obstructive</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Pulmonary Disease, Chronic Obstructive</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Disease Models, Animal</term><term>Endoplasmic Reticulum Stress</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">During the present study, we explored the protective effects of autophagy on endoplasmic reticulum (ER) stress (ERS) induced apoptosis belonging to alveolar epithelial cells (AECs) in rat models with chronic obstructive pulmonary disease (COPD). Fifty-six 12-week-old male Sprague-Dawley (SD) rats were randomly assigned into the COPD group (rats exposed to cigarette smoke (CS)), the 3-methyladenine (3-MA) intervention group (COPD rats were administrated with 10 mg/kg autophagy inhibitors), the chloroquine (CQ)-intervention group (COPD rats were administrated 40 mg/kg CQ), and the control group (rats breathed in normal saline). The forced expiratory volume in 0.3 s/forced vital capacity (FEV<sub>0.3</sub>/FVC%), inspiratory resistance (RI), and dynamic lung compliance (Cdyn) were measured and recorded. The expressions of PKR-like ER kinase (PERK) and CCAAT/enhancer-binding protein-homologous protein (CHOP) were detected by immunohistochemistry. The cell apoptotic rates of AECs were analyzed by terminal deoxynucleotidyl transferase (TdT) mediated dUTP-biotin nick end-labeling (TUNEL) staining. The expression levels of light chain 3 (LC3-II), p62, Beclin-1, ATG5, ATG7, Caspase-12, and Caspase-3 were detected by Western blotting. Results showed that the COPD group exhibited a lower FEV<sub>0.3</sub>/FVC% and Cdyn, and a higher RI than the control group. Compared with the control group, the integrated optical density (IOD) values of PERK and CHOP, the apoptotic rate of AECs, and expressions of LC3-II, Beclin-1, ATG5, ATG7, Caspase-3, and Caspase-12 expressions were significantly higher, whereas p62 expression was significantly lower in the COPD group. Based on the results obtained during the present study, it became clear that the inhibition of autophagy could attenuate the ERS-induced apoptosis of AECs in rats with COPD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28963374</PMID><DateCompleted><Year>2018</Year><Month>06</Month><Day>29</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1573-4935</ISSN><JournalIssue CitedMedium="Internet"><Volume>37</Volume><Issue>6</Issue><PubDate><Year>2017</Year><Month>Dec</Month><Day>22</Day></PubDate></JournalIssue><Title>Bioscience reports</Title><ISOAbbreviation>Biosci. Rep.</ISOAbbreviation></Journal><ArticleTitle>Protective effect of autophagy on endoplasmic reticulum stress induced apoptosis of alveolar epithelial cells in rat models of COPD.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">BSR20170803</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1042/BSR20170803</ELocationID><Abstract><AbstractText>During the present study, we explored the protective effects of autophagy on endoplasmic reticulum (ER) stress (ERS) induced apoptosis belonging to alveolar epithelial cells (AECs) in rat models with chronic obstructive pulmonary disease (COPD). Fifty-six 12-week-old male Sprague-Dawley (SD) rats were randomly assigned into the COPD group (rats exposed to cigarette smoke (CS)), the 3-methyladenine (3-MA) intervention group (COPD rats were administrated with 10 mg/kg autophagy inhibitors), the chloroquine (CQ)-intervention group (COPD rats were administrated 40 mg/kg CQ), and the control group (rats breathed in normal saline). The forced expiratory volume in 0.3 s/forced vital capacity (FEV<sub>0.3</sub>/FVC%), inspiratory resistance (RI), and dynamic lung compliance (Cdyn) were measured and recorded. The expressions of PKR-like ER kinase (PERK) and CCAAT/enhancer-binding protein-homologous protein (CHOP) were detected by immunohistochemistry. The cell apoptotic rates of AECs were analyzed by terminal deoxynucleotidyl transferase (TdT) mediated dUTP-biotin nick end-labeling (TUNEL) staining. The expression levels of light chain 3 (LC3-II), p62, Beclin-1, ATG5, ATG7, Caspase-12, and Caspase-3 were detected by Western blotting. Results showed that the COPD group exhibited a lower FEV<sub>0.3</sub>/FVC% and Cdyn, and a higher RI than the control group. Compared with the control group, the integrated optical density (IOD) values of PERK and CHOP, the apoptotic rate of AECs, and expressions of LC3-II, Beclin-1, ATG5, ATG7, Caspase-3, and Caspase-12 expressions were significantly higher, whereas p62 expression was significantly lower in the COPD group. Based on the results obtained during the present study, it became clear that the inhibition of autophagy could attenuate the ERS-induced apoptosis of AECs in rats with COPD.</AbstractText><CopyrightInformation>© 2017 The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Yao</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cai</LastName><ForeName>Qi-Hang</ForeName><Initials>QH</Initials><AffiliationInfo><Affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yong-Jian</ForeName><Initials>YJ</Initials><AffiliationInfo><Affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fan</LastName><ForeName>Shao-Hua</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Zi-Feng</ForeName><Initials>ZF</Initials><AffiliationInfo><Affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Meng-Qi</ForeName><Initials>MQ</Initials><AffiliationInfo><Affiliation>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Jin-Yu</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Dong-Mei</ForeName><Initials>DM</Initials><AffiliationInfo><Affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zheng</LastName><ForeName>Yuan-Lin</ForeName><Initials>YL</Initials><AffiliationInfo><Affiliation>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China wdm8610@jsnu.edu.cn lu-jun75@163.com ylzheng@jsnu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>11</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Biosci Rep</MedlineTA><NlmUniqueID>8102797</NlmUniqueID><ISSNLinking>0144-8463</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012906">Smoke</NameOfSubstance></Chemical><Chemical><RegistryNumber>5142-23-4</RegistryNumber><NameOfSubstance UI="C025946">3-methyladenine</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance 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MajorTopicYN="Y">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059865" MajorTopicYN="Y">Endoplasmic Reticulum Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D029424" MajorTopicYN="N">Pulmonary Disease, Chronic Obstructive</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012906" MajorTopicYN="N">Smoke</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alveolar epithelial cells</Keyword><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">Chronic obstructive pulmonary disease</Keyword><Keyword MajorTopicYN="N">Endoplasmic reticulum stress</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>05</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>09</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>09</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>6</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28963374</ArticleId><ArticleId IdType="pii">BSR20170803</ArticleId><ArticleId IdType="doi">10.1042/BSR20170803</ArticleId><ArticleId IdType="pmc">PMC5686393</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Toxicology. 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