0 111

Cited 8 times in

ROS-dependent HMGB1 secretion upregulates IL-8 in upper airway epithelial cells under hypoxic condition

DC FieldValueLanguage
dc.contributor.author김경수-
dc.contributor.author김창훈-
dc.contributor.author윤주헌-
dc.date.accessioned2018-07-20T07:55:21Z-
dc.date.available2018-07-20T07:55:21Z-
dc.date.issued2017-
dc.identifier.issn1933-0219-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/160669-
dc.description.abstractHigh-mobility group box 1 (HMGB1) mediates various functions according to the location. We tried to investigate the role of HMGB1 in upper airway under hypoxic conditions. We cultured primary normal human nasal epithelium (NHNE) cells under hypoxic conditions and evaluated the movement of HMGB1 by western blotting, immunofluorescence, and enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS) level was evaluated to estimate the translocation mechanism of HMGB1. The role of secreted HMGB1 was evaluated by ELISA assay. Furthermore, we collected human nasal mucosa samples and nasal lavage fluids from patients conditioned under hypoxic and non-hypoxic environment, and compared the expression of HMGB1 in human nasal mucosa samples by immunohistochemistry and the levels of HMGB1 in lavage fluids using ELISA assay. Hypoxia induced translocation of HMGB1 into the extracellular area and it was dependent on ROS produced by dual oxidase 2. Secreted HMGB1 was involved in the upregulation of interleukin (IL)-8. In human samples, HMGB1 was translocated from nucleus to the cytoplasm in hypoxic-conditioned nasal mucosa. HMGB1 was increased in nasal lavage samples of chronic rhinosinusitis patients, whose sinus mucosa was supposed to be hypoxic as compared with controls. We suggest that HMGB1 is secreted in hypoxic condition via ROS-dependent mechanism and secreted HMGB1 participates in IL-8 upregulation mediating inflammatory response.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherNature Pub. Group-
dc.relation.isPartOfMUCOSAL IMMUNOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdult-
dc.subject.MESHCells, Cultured-
dc.subject.MESHChronic Disease-
dc.subject.MESHDual Oxidases/metabolism-
dc.subject.MESHFemale-
dc.subject.MESHHMGB1 Protein/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHHypoxia/immunology-
dc.subject.MESHInterleukin-8/genetics-
dc.subject.MESHInterleukin-8/metabolism-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHNasal Mucosa/immunology-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHRespiratory Mucosa/immunology-
dc.subject.MESHRhinitis/immunology-
dc.subject.MESHSinusitis/immunology-
dc.subject.MESHUp-Regulation-
dc.subject.MESHYoung Adult-
dc.titleROS-dependent HMGB1 secretion upregulates IL-8 in upper airway epithelial cells under hypoxic condition-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Otorhinolaryngology-
dc.contributor.googleauthorHJ Min-
dc.contributor.googleauthorJ-H Kim-
dc.contributor.googleauthorJE Yoo-
dc.contributor.googleauthorJ-H Oh-
dc.contributor.googleauthorKS Kim-
dc.contributor.googleauthorJ-H Yoon-
dc.contributor.googleauthorC-H Kim-
dc.identifier.doi10.1038/mi.2016.82-
dc.contributor.localIdA00298-
dc.contributor.localIdA01050-
dc.contributor.localIdA02604-
dc.relation.journalcodeJ02276-
dc.identifier.eissn1935-3456-
dc.identifier.pmid27624778-
dc.identifier.urlhttp://www.nature.com/articles/mi201682-
dc.contributor.alternativeNameKim, Kyung Su-
dc.contributor.alternativeNameKim, Chang Hoon-
dc.contributor.alternativeNameYoon, Joo Heon-
dc.contributor.affiliatedAuthorKim, Kyung Su-
dc.contributor.affiliatedAuthorKim, Chang Hoon-
dc.contributor.affiliatedAuthorYoon, Joo Heon-
dc.citation.volume10-
dc.citation.number3-
dc.citation.startPage685-
dc.citation.endPage694-
dc.identifier.bibliographicCitationMUCOSAL IMMUNOLOGY, Vol.10(3) : 685-694, 2017-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.