Protective effect of autophagy on endoplasmic reticulum stress induced apoptosis of alveolar epithelial cells in rat models of COPD.
Identifieur interne : 000C99 ( Main/Exploration ); précédent : 000C98; suivant : 000D00Protective effect of autophagy on endoplasmic reticulum stress induced apoptosis of alveolar epithelial cells in rat models of COPD.
Auteurs : Yao Tang [République populaire de Chine] ; Qi-Hang Cai [République populaire de Chine] ; Yong-Jian Wang [République populaire de Chine] ; Shao-Hua Fan [République populaire de Chine] ; Zi-Feng Zhang [République populaire de Chine] ; Meng-Qi Xiao [République populaire de Chine] ; Jin-Yu Zhu [République populaire de Chine] ; Dong-Mei Wu ; Jun Lu ; Yuan-Lin ZhengSource :
- Bioscience reports [ 1573-4935 ] ; 2017.
Descripteurs français
- KwdFr :
- Adénine (analogues et dérivés), Adénine (pharmacologie), Animaux, Apoptose, Autophagie (), Broncho-pneumopathie chronique obstructive (), Broncho-pneumopathie chronique obstructive (anatomopathologie), Broncho-pneumopathie chronique obstructive (physiopathologie), Chloroquine (pharmacologie), Fumée (effets indésirables), Marqueurs biologiques (métabolisme), Modèles animaux de maladie humaine, Mâle, Pneumocytes (), Pneumocytes (anatomopathologie), Rat Sprague-Dawley, Rats, Stress du réticulum endoplasmique.
- MESH :
- analogues et dérivés : Adénine.
- anatomopathologie : Broncho-pneumopathie chronique obstructive, Pneumocytes.
- effets indésirables : Fumée.
- métabolisme : Marqueurs biologiques.
- pharmacologie : Adénine, Chloroquine.
- physiopathologie : Broncho-pneumopathie chronique obstructive.
- Animaux, Apoptose, Autophagie, Broncho-pneumopathie chronique obstructive, Modèles animaux de maladie humaine, Mâle, Pneumocytes, Rat Sprague-Dawley, Rats, Stress du réticulum endoplasmique.
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
Affiliations:
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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116</wicri:regionArea><wicri:noRegion>Xuzhou 221116</wicri:noRegion></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 wicri:level="1"><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><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116</wicri:regionArea><wicri:noRegion>Xuzhou 221116</wicri:noRegion></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 wicri:level="1"><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><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116</wicri:regionArea><wicri:noRegion>Xuzhou 221116</wicri:noRegion></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 wicri:level="1"><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><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116</wicri:regionArea><wicri:noRegion>Xuzhou 221116</wicri:noRegion></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 wicri:level="1"><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><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116</wicri:regionArea><wicri:noRegion>Xuzhou 221116</wicri:noRegion></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 wicri:level="1"><nlm:affiliation>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000</wicri:regionArea><wicri:noRegion>Kaifeng 475000</wicri:noRegion></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 wicri:level="1"><nlm:affiliation>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Respiration, Huaihe Hospital of Henan University, Kaifeng 475000</wicri:regionArea><wicri:noRegion>Kaifeng 475000</wicri:noRegion></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><wicri:noCountry code="subField">P.R.</wicri:noCountry></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><wicri:noCountry code="subField">P.R.</wicri:noCountry></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><wicri:noCountry code="subField">P.R.</wicri:noCountry></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="KwdFr" xml:lang="fr"><term>Adénine (analogues et dérivés)</term><term>Adénine (pharmacologie)</term><term>Animaux</term><term>Apoptose</term><term>Autophagie ()</term><term>Broncho-pneumopathie chronique obstructive ()</term><term>Broncho-pneumopathie chronique obstructive (anatomopathologie)</term><term>Broncho-pneumopathie chronique obstructive (physiopathologie)</term><term>Chloroquine (pharmacologie)</term><term>Fumée (effets indésirables)</term><term>Marqueurs biologiques (métabolisme)</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Pneumocytes ()</term><term>Pneumocytes (anatomopathologie)</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Stress du réticulum endoplasmique</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="analogues et dérivés" xml:lang="fr"><term>Adénine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Broncho-pneumopathie chronique obstructive</term><term>Pneumocytes</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="effets indésirables" xml:lang="fr"><term>Fumée</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Marqueurs biologiques</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="pharmacologie" xml:lang="fr"><term>Adénine</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Broncho-pneumopathie chronique 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><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Broncho-pneumopathie chronique obstructive</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Pneumocytes</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Stress du réticulum endoplasmique</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><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Lu, Jun" sort="Lu, Jun" uniqKey="Lu J" first="Jun" last="Lu">Jun Lu</name><name sortKey="Wu, Dong Mei" sort="Wu, Dong Mei" uniqKey="Wu D" first="Dong-Mei" last="Wu">Dong-Mei Wu</name><name sortKey="Zheng, Yuan Lin" sort="Zheng, Yuan Lin" uniqKey="Zheng Y" first="Yuan-Lin" last="Zheng">Yuan-Lin Zheng</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Tang, Yao" sort="Tang, Yao" uniqKey="Tang Y" first="Yao" last="Tang">Yao Tang</name></noRegion><name sortKey="Cai, Qi Hang" sort="Cai, Qi Hang" uniqKey="Cai Q" first="Qi-Hang" last="Cai">Qi-Hang Cai</name><name sortKey="Fan, Shao Hua" sort="Fan, Shao Hua" uniqKey="Fan S" first="Shao-Hua" last="Fan">Shao-Hua Fan</name><name sortKey="Wang, Yong Jian" sort="Wang, Yong Jian" uniqKey="Wang Y" first="Yong-Jian" last="Wang">Yong-Jian Wang</name><name sortKey="Xiao, Meng Qi" sort="Xiao, Meng Qi" uniqKey="Xiao M" first="Meng-Qi" last="Xiao">Meng-Qi Xiao</name><name sortKey="Zhang, Zi Feng" sort="Zhang, Zi Feng" uniqKey="Zhang Z" first="Zi-Feng" last="Zhang">Zi-Feng Zhang</name><name sortKey="Zhu, Jin Yu" sort="Zhu, Jin Yu" uniqKey="Zhu J" first="Jin-Yu" last="Zhu">Jin-Yu Zhu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:28963374" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |