Effect of Cadmium on Human Middle Ear Epithelial Cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Song, Jae Jun | - |
dc.contributor.author | Kim, Ju Yeon | - |
dc.contributor.author | Jang, An Soo | - |
dc.contributor.author | Kim, Shin Hye | - |
dc.contributor.author | Rah, Yoon Chan | - |
dc.contributor.author | Park, Mina | - |
dc.contributor.author | Park, Moo Kyun | - |
dc.date.accessioned | 2021-09-04T10:10:16Z | - |
dc.date.available | 2021-09-04T10:10:16Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2015-12 | - |
dc.identifier.issn | 1308-7649 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/91775 | - |
dc.description.abstract | OBJECTIVE: Cadmium (Cd2+) exposure can occur through passive smoking, ambient air pollution, and food. Even low exposure can affect hearing and cause lung disease. Here we investigated whether cadmium causes cytotoxicity induces inflammation, or increases mucin gene expression in immortalized human middle ear epithelial cells (HMEECs). MATERIALS and METHODS: Cell viability was investigated using the MTT assay following Cd2+ treatment increases in apoptosis and necrosis were determined and the production of reactive oxygen species (ROS) was measure. We analyzed the expression of an inflammatory cytokine (COX-2) gene and a mucin gene (MUC5AC) using RT-PCR. RESULTS: Exposure to >20 mu M Cd2+ caused a significant decrease in cell viability Hoechst 33258 staining showed apoptotic morphology of heterogeneous intensity, condensation, and fragmentation after Cd2+ exposure, Cd2+ was shown to increase cell death by apoptosis and necrosis and necrosis by annexin V-FITC/PI double staining Cd2+ exposure increased ROS production and COX-2 and MUC5AC expressions. CONCLUSION: Our findings suggest that environmental cadmium exposure is related to the development of otitis media. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | AVES | - |
dc.subject | OTITIS-MEDIA | - |
dc.subject | IN-VITRO | - |
dc.subject | EXPRESSION | - |
dc.subject | APOPTOSIS | - |
dc.subject | CYTOKINES | - |
dc.subject | TOXICITY | - |
dc.subject | RELEASE | - |
dc.subject | REPAIR | - |
dc.title | Effect of Cadmium on Human Middle Ear Epithelial Cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Song, Jae Jun | - |
dc.contributor.affiliatedAuthor | Rah, Yoon Chan | - |
dc.identifier.doi | 10.5152/iao.2015.756 | - |
dc.identifier.scopusid | 2-s2.0-84975705119 | - |
dc.identifier.wosid | 000371282300002 | - |
dc.identifier.bibliographicCitation | JOURNAL OF INTERNATIONAL ADVANCED OTOLOGY, v.11, no.3, pp.183 - 187 | - |
dc.relation.isPartOf | JOURNAL OF INTERNATIONAL ADVANCED OTOLOGY | - |
dc.citation.title | JOURNAL OF INTERNATIONAL ADVANCED OTOLOGY | - |
dc.citation.volume | 11 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 183 | - |
dc.citation.endPage | 187 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Otorhinolaryngology | - |
dc.relation.journalWebOfScienceCategory | Otorhinolaryngology | - |
dc.subject.keywordPlus | OTITIS-MEDIA | - |
dc.subject.keywordPlus | IN-VITRO | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | CYTOKINES | - |
dc.subject.keywordPlus | TOXICITY | - |
dc.subject.keywordPlus | RELEASE | - |
dc.subject.keywordPlus | REPAIR | - |
dc.subject.keywordAuthor | Cadmium | - |
dc.subject.keywordAuthor | human middle ear epithelial cells | - |
dc.subject.keywordAuthor | otitis media | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.