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Clusterin Deficiency Exacerbates Hyperoxia-Induced Acute Lung Injury
DC Field | Value | Language |
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dc.contributor.author | 김경원 | - |
dc.contributor.author | 김미나 | - |
dc.contributor.author | 김수연 | - |
dc.contributor.author | 김윤희 | - |
dc.contributor.author | 손명현 | - |
dc.contributor.author | 이순민 | - |
dc.contributor.author | 홍정연 | - |
dc.date.accessioned | 2021-05-26T17:01:35Z | - |
dc.date.available | 2021-05-26T17:01:35Z | - |
dc.date.issued | 2021-04 | - |
dc.identifier.issn | 2073-4409 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/182956 | - |
dc.description.abstract | Exposure to high oxygen concentrations leads to generation of excessive reactive oxygen species, causing cellular injury and multiple organ dysfunctions and is associated with a high mortality rate. Clusterin (CLU) is a heterodimeric glycoprotein that mediates several intracellular signaling pathways, including cell death and inflammation. However, the role of CLU in the pathogenesis of hyperoxic acute lung injury (HALI) is unknown. Wild-type (WT) and CLU-deficient mice and cultured human airway epithelial cells were used. Changes in cell death- and inflammation-related molecules with or without hyperoxia exposure in cells and animals were determined. Hyperoxia induced an increase in CLU expression in mouse lungs and human airway epithelial cells. Mice lacking CLU had increased HALI and mortality rate compared with WT mice. In vitro, CLU-disrupted cells showed enhanced release of cytochrome c, Bax translocation, cell death and inflammatory cytokine expression. However, treatment with recombinant CLU attenuated hyperoxia-induced apoptosis. Moreover, the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analyses revealed metabolic pathways, hematopoietic cell lineage, response to stress and localization and regulation of immune system that were differentially regulated between WT and CLU-/- mice. These results demonstrate that prolonged hyperoxia-induced lung injury is associated with CLU expression and that CLU replenishment may alleviate hyperoxia-induced cell death. | - |
dc.description.statementOfResponsibility | open | - |
dc.language | English | - |
dc.publisher | MDPI | - |
dc.relation.isPartOf | CELLS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.title | Clusterin Deficiency Exacerbates Hyperoxia-Induced Acute Lung Injury | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | ;Dept. of Pediatrics (소아과학교실) | - |
dc.contributor.googleauthor | Jung Yeon Hong | - |
dc.contributor.googleauthor | Mi Na Kim | - |
dc.contributor.googleauthor | Eun Gyul Kim | - |
dc.contributor.googleauthor | Jae Woo Lee | - |
dc.contributor.googleauthor | Hye Rin Kim | - |
dc.contributor.googleauthor | Soo Yeon Kim | - |
dc.contributor.googleauthor | Soon Min Lee | - |
dc.contributor.googleauthor | Yoon Hee Kim | - |
dc.contributor.googleauthor | Kyung Won Kim | - |
dc.contributor.googleauthor | Myung Hyun Sohn | - |
dc.identifier.doi | 10.3390/cells10040944 | - |
dc.contributor.localId | A00303 | - |
dc.contributor.localId | A00441 | - |
dc.contributor.localId | A04724 | - |
dc.contributor.localId | A00799 | - |
dc.contributor.localId | A01967 | - |
dc.contributor.localId | A02905 | - |
dc.contributor.localId | A04431 | - |
dc.relation.journalcode | J03774 | - |
dc.identifier.pmid | 33921872 | - |
dc.subject.keyword | acute lung injury | - |
dc.subject.keyword | apoptosis | - |
dc.subject.keyword | clusterin | - |
dc.subject.keyword | hyperoxia | - |
dc.subject.keyword | inflammation | - |
dc.contributor.alternativeName | Kim, Kyung Won | - |
dc.contributor.affiliatedAuthor | 김경원 | - |
dc.contributor.affiliatedAuthor | 김미나 | - |
dc.contributor.affiliatedAuthor | 김수연 | - |
dc.contributor.affiliatedAuthor | 김윤희 | - |
dc.contributor.affiliatedAuthor | 손명현 | - |
dc.contributor.affiliatedAuthor | 이순민 | - |
dc.contributor.affiliatedAuthor | 홍정연 | - |
dc.citation.volume | 10 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 944 | - |
dc.identifier.bibliographicCitation | CELLS, Vol.10(4) : 944, 2021-04 | - |
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