Cited 112 times in
Carbon monoxide activates autophagy via mitochondrial reactive oxygen species formation
DC Field | Value | Language |
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dc.contributor.author | 김영삼 | - |
dc.date.accessioned | 2014-12-20T17:39:25Z | - |
dc.date.available | 2014-12-20T17:39:25Z | - |
dc.date.issued | 2011 | - |
dc.identifier.issn | 1044-1549 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/95014 | - |
dc.description.abstract | Autophagy, an autodigestive process that degrades cellular organelles and protein, plays an important role in maintaining cellular homeostasis during environmental stress. Carbon monoxide (CO), a toxic gas and candidate therapeutic molecule, confers cytoprotection in animal models of acute lung injury. The mechanisms underlying CO-dependent lung cell protection and the role of autophagy in this process remain unclear. Here, we demonstrate that CO exposure time-dependently increased the expression and activation of the autophagic protein, microtubule-associated protein-1 light chain-3B (LC3B) in mouse lung, and in cultured human alveolar (A549) or human bronchial epithelial cells. Furthermore, CO increased autophagosome formation in epithelial cells by electron microscopy and green fluorescent protein (GFP)-LC3 puncta assays. Recent studies indicate that reactive oxygen species (ROS) play an important role in the activation of autophagy. CO up-regulated mitochondria-dependent generation of ROS in epithelial cells, as assayed by MitoSOX fluorescence. Furthermore, CO-dependent induction of LC3B expression was inhibited by N-acetyl-L-cysteine and the mitochondria-targeting antioxidant, Mito-TEMPO. These data suggest that CO promotes the autophagic process through mitochondrial ROS generation. We investigated the relationships between autophagic proteins and CO-dependent cytoprotection using a model of hyperoxic stress. CO protected against hyperoxia-induced cell death, and inhibited hyperoxia-associated ROS production. The ability of CO to protect against hyperoxia-induced cell death and caspase-3 activation was compromised in epithelial cells infected with LC3B-small interfering (si)RNA, indicating a role for autophagic proteins. These studies uncover a new mechanism for the protective action of CO, in support of potential therapeutic application of this gas. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 867~873 | - |
dc.relation.isPartOf | AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Administration, Inhalation | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Antioxidants/pharmacology | - |
dc.subject.MESH | Autophagy/drug effects* | - |
dc.subject.MESH | Carbon Monoxide/administration & dosage | - |
dc.subject.MESH | Carbon Monoxide/pharmacology* | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Cytoprotection | - |
dc.subject.MESH | Disease Models, Animal | - |
dc.subject.MESH | Epithelial Cells/drug effects* | - |
dc.subject.MESH | Epithelial Cells/metabolism | - |
dc.subject.MESH | Epithelial Cells/pathology | - |
dc.subject.MESH | Gases | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Hyperoxia/metabolism | - |
dc.subject.MESH | Hyperoxia/pathology | - |
dc.subject.MESH | Hyperoxia/prevention & control* | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Inbred C57BL | - |
dc.subject.MESH | Microscopy, Fluorescence | - |
dc.subject.MESH | Microtubule-Associated Proteins/genetics | - |
dc.subject.MESH | Microtubule-Associated Proteins/metabolism | - |
dc.subject.MESH | Mitochondria/drug effects* | - |
dc.subject.MESH | Mitochondria/metabolism | - |
dc.subject.MESH | Mitochondria/pathology | - |
dc.subject.MESH | Oxidative Stress/drug effects* | - |
dc.subject.MESH | RNA Interference | - |
dc.subject.MESH | Reactive Oxygen Species/metabolism* | - |
dc.subject.MESH | Respiratory Mucosa/drug effects* | - |
dc.subject.MESH | Respiratory Mucosa/metabolism | - |
dc.subject.MESH | Respiratory Mucosa/pathology | - |
dc.subject.MESH | Signal Transduction/drug effects | - |
dc.subject.MESH | Time Factors | - |
dc.subject.MESH | Transfection | - |
dc.title | Carbon monoxide activates autophagy via mitochondrial reactive oxygen species formation | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Seon-Jin Lee | - |
dc.contributor.googleauthor | Stefan W. Ryter | - |
dc.contributor.googleauthor | Jin-Fu Xu | - |
dc.contributor.googleauthor | Kiichi Nakahira | - |
dc.contributor.googleauthor | Hong Pyo Kim | - |
dc.contributor.googleauthor | Augustine M. K. Choi | - |
dc.contributor.googleauthor | Young Sam Kim | - |
dc.identifier.doi | 10.1165/rcmb.2010-0352OC | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00707 | - |
dc.relation.journalcode | J00113 | - |
dc.identifier.eissn | 1535-4989 | - |
dc.identifier.pmid | 21441382 | - |
dc.subject.keyword | apoptosis | - |
dc.subject.keyword | autophagy | - |
dc.subject.keyword | carbon monoxide | - |
dc.subject.keyword | epithelial cells | - |
dc.subject.keyword | hyperoxia | - |
dc.contributor.alternativeName | Kim, Young Sam | - |
dc.contributor.affiliatedAuthor | Kim, Young Sam | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 45 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 867 | - |
dc.citation.endPage | 873 | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol.45(4) : 867-873, 2011 | - |
dc.identifier.rimsid | 26980 | - |
dc.type.rims | ART | - |
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