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Cited 18 times in

Dual Oxidase 2 in Lung Epithelia Is Essential for Hyperoxia-Induced Acute Lung Injury in Mice

DC FieldValueLanguage
dc.contributor.author권영희-
dc.contributor.author김민지-
dc.contributor.author류재찬-
dc.contributor.author유지환-
dc.contributor.author윤주헌-
dc.date.accessioned2015-01-06T17:30:51Z-
dc.date.available2015-01-06T17:30:51Z-
dc.date.issued2014-
dc.identifier.issn1523-0864-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/100120-
dc.description.abstractAims: Acute lung injury (ALI) induced by excessive hyperoxia has been employed as a model of oxidative stress imitating acute respiratory distress syndrome. Under hyperoxic conditions, overloading quantities of reactive oxygen species (ROS) are generated in both lung epithelial and endothelial cells, leading to ALI. Some NADPH oxidase (NOX) family enzymes are responsible for hyperoxia-induced ROS generation in lung epithelial and endothelial cells. However, the molecular mechanisms of ROS production in type II alveolar epithelial cells (AECs) and ALI induced by hyperoxia are poorly understood. Results: In this study, we show that dual oxidase 2 (DUOX2) is a key NOX enzyme that affects hyperoxia-induced ROS production, particularly in type II AECs, leading to lung injury. In DUOX2 mutant mice (DUOX2thyd/thyd) or mice in which DUOX2 expression is knocked down in the lungs, hyperoxia-induced ALI was significantly lower than in wild-type (WT) mice. DUOX2 was mainly expressed in type II AECs, but not endothelial cells, and hyperoxia-induced ROS production was markedly reduced in primary type II AECs isolated from DUOX2thyd/thyd mice. Furthermore, DUOX2-generated ROS are responsible for caspase-mediated cell death, inducing ERK and JNK phophorylation in type II AECs. Innovation: To date, no role for DUOX2 has been defined in hyperoxia-mediated ALI despite it being a NOX homologue and major ROS source in lung epithelium. Conclusion: Here, we present the novel finding that DUOX2-generated ROS induce AEC death, leading to hyperoxia-induced lung injury.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1803~1818-
dc.relation.isPartOfANTIOXIDANTS & REDOX SIGNALING-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAcute Lung Injury/metabolism*-
dc.subject.MESHAcute Lung Injury/pathology-
dc.subject.MESHAnimals-
dc.subject.MESHCaspases/metabolism-
dc.subject.MESHCell Death/physiology-
dc.subject.MESHDual Oxidases-
dc.subject.MESHEndothelial Cells/metabolism-
dc.subject.MESHEndothelial Cells/pathology-
dc.subject.MESHEpithelial Cells/metabolism-
dc.subject.MESHEpithelial Cells/pathology-
dc.subject.MESHHyperoxia/metabolism*-
dc.subject.MESHLung/cytology-
dc.subject.MESHLung/metabolism*-
dc.subject.MESHMAP Kinase Signaling System/physiology-
dc.subject.MESHMice-
dc.subject.MESHNADPH Oxidases/metabolism*-
dc.subject.MESHOxidative Stress/physiology-
dc.subject.MESHPhosphorylation/physiology-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.titleDual Oxidase 2 in Lung Epithelia Is Essential for Hyperoxia-Induced Acute Lung Injury in Mice-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentYonsei Biomedical Research Center (연세의생명연구원)-
dc.contributor.googleauthorKim Min-Ji-
dc.contributor.googleauthorRyu Jae-Chan-
dc.contributor.googleauthorKwon Younghee-
dc.contributor.googleauthorLee Suhee-
dc.contributor.googleauthorBae Yun Soo-
dc.contributor.googleauthorYoon Joo-Heon-
dc.contributor.googleauthorRyu Ji-Hwan-
dc.identifier.doi10.1089/ars.2013.5677-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00233-
dc.contributor.localIdA01329-
dc.contributor.localIdA02604-
dc.contributor.localIdA00477-
dc.contributor.localIdA02522-
dc.relation.journalcodeJ00190-
dc.identifier.eissn1557-7716-
dc.identifier.pmid24766345-
dc.contributor.alternativeNameKwon, Younghee-
dc.contributor.alternativeNameKim, Min Ji-
dc.contributor.alternativeNameRyu, Jae Chan-
dc.contributor.alternativeNameRyu, Ji Hwan-
dc.contributor.alternativeNameYoon, Joo Heon-
dc.contributor.affiliatedAuthorKwon, Younghee-
dc.contributor.affiliatedAuthorRyu, Jae Chan-
dc.contributor.affiliatedAuthorYoon, Joo Heon-
dc.contributor.affiliatedAuthorKim, Min Ji-
dc.contributor.affiliatedAuthorRyu, Ji Hwan-
dc.citation.volume21-
dc.citation.number13-
dc.citation.startPage1803-
dc.citation.endPage1818-
dc.identifier.bibliographicCitationANTIOXIDANTS & REDOX SIGNALING, Vol.21(13) : 1803-1818, 2014-
Appears in Collections:
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Research Center for Human Natural Defense System (생체방어연구센터) > 1. Journal Papers

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