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The chitinase-like proteins breast regression protein-39 and YKL-40 regulate hyperoxia-induced acute lung injury.
DC Field | Value | Language |
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dc.contributor.author | 손명현 | - |
dc.date.accessioned | 2015-04-23T17:22:24Z | - |
dc.date.available | 2015-04-23T17:22:24Z | - |
dc.date.issued | 2010 | - |
dc.identifier.issn | 1073-449X | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/102337 | - |
dc.description.abstract | RATIONALE: Prolonged exposure to 100% O(2) causes hyperoxic acute lung injury (HALI), characterized by alveolar epithelial cell injury and death. We previously demonstrated that the murine chitinase-like protein, breast regression protein (BRP)-39 and its human homolog, YKL-40, inhibit cellular apoptosis. However, the regulation and roles of these molecules in hyperoxia have not been addressed. OBJECTIVES: We hypothesized that BRP-39 and YKL-40 (also called chitinase-3-like 1) play important roles in the pathogenesis of HALI. METHODS: We characterized the regulation of BRP-39 during HALI and the responses induced by hyperoxia in wild-type mice, BRP-39-null (-/-) mice, and BRP-39(-/-) mice in which YKL-40 was overexpressed in respiratory epithelium. We also compared the levels of tracheal aspirate YKL-40 in premature newborns with respiratory failure. MEASUREMENTS AND MAIN RESULTS: These studies demonstrate that hyperoxia inhibits BRP-39 in vivo in the murine lung and in vitro in epithelial cells. They also demonstrate that BRP-39(-/-) mice have exaggerated permeability, protein leak, oxidation, inflammatory, chemokine, and epithelial apoptosis responses, and experience premature death in 100% O(2). Lastly, they demonstrate that YKL-40 ameliorates HALI, prolongs survival in 100% O(2), and rescues the exaggerated injury response in BRP-39(-/-) animals. In accord with these findings, the levels of tracheal aspirate YKL-40 were lower in premature infants treated with hyperoxia for respiratory failure who subsequently experienced bronchopulmonary dysplasia or death compared with those that did not experience these complications. CONCLUSIONS: These studies demonstrate that hyperoxia inhibits BRP-39/YKL-40, and that BRP-39 and YKL-40 are critical regulators of oxidant injury, inflammation, and epithelial apoptosis in the murine and human lung | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 918~928 | - |
dc.relation.isPartOf | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE | - |
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 | Acute Lung Injury/physiopathology* | - |
dc.subject.MESH | Adipokines | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Apoptosis | - |
dc.subject.MESH | Bronchopulmonary Dysplasia/physiopathology* | - |
dc.subject.MESH | Cells, Cultured | - |
dc.subject.MESH | Chitinase-3-Like Protein 1 | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Glycoproteins/metabolism* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Hyperoxia/physiopathology* | - |
dc.subject.MESH | Infant, Newborn | - |
dc.subject.MESH | Infant, Premature* | - |
dc.subject.MESH | Inflammation | - |
dc.subject.MESH | Lectins/metabolism* | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Transgenic | - |
dc.subject.MESH | Respiratory Mucosa/metabolism | - |
dc.subject.MESH | Survival Analysis | - |
dc.title | The chitinase-like proteins breast regression protein-39 and YKL-40 regulate hyperoxia-induced acute lung injury. | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Pediatrics (소아과학) | - |
dc.contributor.googleauthor | Myung Hyun Sohn | - |
dc.contributor.googleauthor | Min-Jong Kang | - |
dc.contributor.googleauthor | Hiroshi Matsuura | - |
dc.contributor.googleauthor | Vineet Bhandari | - |
dc.contributor.googleauthor | Ning-Yuan Chen | - |
dc.contributor.googleauthor | Chun Geun Lee | - |
dc.contributor.googleauthor | Jack A. Elias | - |
dc.identifier.doi | 10.1164/rccm.200912-1793OC | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01967 | - |
dc.relation.journalcode | J00112 | - |
dc.identifier.eissn | 1535-4970 | - |
dc.identifier.pmid | 20558631 | - |
dc.subject.keyword | BRP-39 | - |
dc.subject.keyword | YKL-40 | - |
dc.subject.keyword | hyperoxygen | - |
dc.subject.keyword | BPD | - |
dc.subject.keyword | HALI | - |
dc.contributor.alternativeName | Son, Myung Hyun | - |
dc.contributor.affiliatedAuthor | Son, Myung Hyun | - |
dc.citation.volume | 182 | - |
dc.citation.number | 7 | - |
dc.citation.startPage | 918 | - |
dc.citation.endPage | 928 | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol.182(7) : 918-928, 2010 | - |
dc.identifier.rimsid | 40867 | - |
dc.type.rims | ART | - |
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