Integrin αvβ5 inhibition protects against ischemia-reperfusion-induced lung injury in an autophagy-dependent manner.
Identifieur interne : 000D11 ( Main/Exploration ); précédent : 000D10; suivant : 000D12Integrin αvβ5 inhibition protects against ischemia-reperfusion-induced lung injury in an autophagy-dependent manner.
Auteurs : Dan Zhang [République populaire de Chine] ; Chichi Li [République populaire de Chine] ; Yuanlin Song [République populaire de Chine] ; Jian Zhou [République populaire de Chine] ; Yuping Li [République populaire de Chine] ; Jing Li [République populaire de Chine] ; Chunxue Bai [République populaire de Chine]Source :
- American journal of physiology. Lung cellular and molecular physiology [ 1522-1504 ] ; 2017.
Descripteurs français
- KwdFr :
- Agents protecteurs (pharmacologie), Animaux, Apoptose (), Autophagie (), Caspase-3 (métabolisme), Cellules cultivées, Cellules endothéliales (), Cellules endothéliales (métabolisme), Glucose (métabolisme), Humains, Liquide de lavage bronchoalvéolaire (), Lésion d'ischémie-reperfusion (métabolisme), Lésion d'ischémie-reperfusion (traitement médicamenteux), Lésion pulmonaire aigüe (métabolisme), Lésion pulmonaire aigüe (traitement médicamenteux), Oxygène (métabolisme), Poumon (), Poumon (métabolisme), Récepteur vitronectine (antagonistes et inhibiteurs), Récepteur vitronectine (métabolisme), Souris, Souris de lignée C57BL.
- MESH :
- antagonistes et inhibiteurs : Récepteur vitronectine.
- métabolisme : Caspase-3, Cellules endothéliales, Glucose, Lésion d'ischémie-reperfusion, Lésion pulmonaire aigüe, Oxygène, Poumon, Récepteur vitronectine.
- pharmacologie : Agents protecteurs.
- traitement médicamenteux : Lésion d'ischémie-reperfusion, Lésion pulmonaire aigüe.
- Animaux, Apoptose, Autophagie, Cellules cultivées, Cellules endothéliales, Humains, Liquide de lavage bronchoalvéolaire, Poumon, Souris, Souris de lignée C57BL.
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
Affiliations:
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Le document en format XML
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Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province</wicri:regionArea><wicri:noRegion>Zhejiang Province</wicri:noRegion></affiliation></author><author><name sortKey="Song, Yuanlin" sort="Song, Yuanlin" uniqKey="Song Y" first="Yuanlin" last="Song">Yuanlin Song</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Li, Yuping" sort="Li, Yuping" uniqKey="Li Y" first="Yuping" last="Li">Yuping Li</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, 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Province</wicri:noRegion></affiliation></author><author><name sortKey="Li, Chichi" sort="Li, Chichi" uniqKey="Li C" first="Chichi" last="Li">Chichi Li</name><affiliation wicri:level="1"><nlm:affiliation>Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province</wicri:regionArea><wicri:noRegion>Zhejiang Province</wicri:noRegion></affiliation></author><author><name sortKey="Song, Yuanlin" sort="Song, Yuanlin" uniqKey="Song Y" first="Yuanlin" last="Song">Yuanlin Song</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Li, Yuping" sort="Li, Yuping" uniqKey="Li Y" first="Yuping" last="Li">Yuping Li</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province</wicri:regionArea><wicri:noRegion>Zhejiang Province</wicri:noRegion></affiliation></author><author><name sortKey="Li, Jing" sort="Li, Jing" uniqKey="Li J" first="Jing" last="Li">Jing Li</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Bai, Chunxue" sort="Bai, Chunxue" uniqKey="Bai C" first="Chunxue" last="Bai">Chunxue Bai</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China; cxbai@fudan.edu.cn.</nlm:affiliation><country wicri:rule="url">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></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="KwdFr" xml:lang="fr"><term>Agents protecteurs (pharmacologie)</term><term>Animaux</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Caspase-3 (métabolisme)</term><term>Cellules cultivées</term><term>Cellules endothéliales ()</term><term>Cellules endothéliales (métabolisme)</term><term>Glucose (métabolisme)</term><term>Humains</term><term>Liquide de lavage bronchoalvéolaire ()</term><term>Lésion d'ischémie-reperfusion (métabolisme)</term><term>Lésion d'ischémie-reperfusion (traitement médicamenteux)</term><term>Lésion pulmonaire aigüe (métabolisme)</term><term>Lésion pulmonaire aigüe (traitement médicamenteux)</term><term>Oxygène (métabolisme)</term><term>Poumon ()</term><term>Poumon (métabolisme)</term><term>Récepteur vitronectine (antagonistes et inhibiteurs)</term><term>Récepteur vitronectine (métabolisme)</term><term>Souris</term><term>Souris de lignée C57BL</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="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteur vitronectine</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" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term><term>Cellules endothéliales</term><term>Glucose</term><term>Lésion d'ischémie-reperfusion</term><term>Lésion pulmonaire aigüe</term><term>Oxygène</term><term>Poumon</term><term>Récepteur vitronectine</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Agents protecteurs</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Protective Agents</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Lésion d'ischémie-reperfusion</term><term>Lésion pulmonaire aigüe</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><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Cellules cultivées</term><term>Cellules endothéliales</term><term>Humains</term><term>Liquide de lavage bronchoalvéolaire</term><term>Poumon</term><term>Souris</term><term>Souris de lignée 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><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Dan" sort="Zhang, Dan" uniqKey="Zhang D" first="Dan" last="Zhang">Dan Zhang</name></noRegion><name sortKey="Bai, Chunxue" sort="Bai, Chunxue" uniqKey="Bai C" first="Chunxue" last="Bai">Chunxue Bai</name><name sortKey="Li, Chichi" sort="Li, Chichi" uniqKey="Li C" first="Chichi" last="Li">Chichi Li</name><name sortKey="Li, Jing" sort="Li, Jing" uniqKey="Li J" first="Jing" last="Li">Jing Li</name><name sortKey="Li, Yuping" sort="Li, Yuping" uniqKey="Li Y" first="Yuping" last="Li">Yuping Li</name><name sortKey="Song, Yuanlin" sort="Song, Yuanlin" uniqKey="Song Y" first="Yuanlin" last="Song">Yuanlin Song</name><name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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