SIRT1 Protects Against Particulate Matter-Induced Oxidative Stress in Human Corneal and Conjunctival Epithelial Cells
DC Field | Value | Language |
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dc.contributor.author | Li, Xiangzhe | - |
dc.contributor.author | Kang, Boram | - |
dc.contributor.author | Eom, Youngsub | - |
dc.contributor.author | Zhong, Jingxiang | - |
dc.contributor.author | Lee, Hyung Keun | - |
dc.contributor.author | Kim, Hyo Myung | - |
dc.contributor.author | Song, Jong Suk | - |
dc.date.accessioned | 2022-12-09T14:41:57Z | - |
dc.date.available | 2022-12-09T14:41:57Z | - |
dc.date.created | 2022-12-08 | - |
dc.date.issued | 2022-09 | - |
dc.identifier.issn | 0146-0404 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/146607 | - |
dc.description.abstract | PURPOSE. Sirtuin1 (SIRT1) as a hot therapeutic target for oxidative stress-associated diseases that has been extensively studied. This study aimed to determine the changes in SIRT1 expression in particulate matter (PM)-induced corneal and conjunctival epithelial cell damage and explore potential drugs to reduce PM-associated ocular surface injury. METHODS. Immortalized human corneal epithelial cells (HCECs) and human conjunctival epithelial cells (HCjECs) were exposed to an ambient PM sample. Cytotoxicity was evaluated by water-soluble tetrazolium salt-8 assay. SIRT1 expression was measured by Western blot analysis. Reactive oxygen species (ROS) production, cell apoptosis, mitochondrial function, and cell senescence were assessed by using 2',7'-dichlorofluorescein diacetate assay, annexin V apoptosis assay, tetramethylrhodamine ethyl ester assay, and senescence beta-galactosidase staining, respectively. RESULTS. PM-induced cytotoxicity of HCECs and HCjECs occurred in a dose-dependent manner. Increased ROS production, as well as decreased SIRT1 expression, were observed in HCECs and HCjECs after 200 mu g/mL PM exposure. In addition, PM induced oxidative stress-mediated cellular damage, including cell apoptosis, mitochondrial damage, and cell senescence. Interestingly, SRT1720, a SIRT1 activator, increased SIRT1 expression and decreased ROS production and attenuated PM-induced cell damage in HCECs and HCjECs. CONCLUSIONS. This study determined that SIRT1 was involved in PM-induced oxidative stress in HCECs and HCjECs and found that ROS overproduction may a key factor in PM-induced SIRT1 downregulation. The SIRT1 activator, SRT1720, can effectively upregulate SIRT1 expression and inhibit ROS production, thereby reversing PM-induced cell damage. This study provides a new potential target for clinical treatment of PM-associated ocular surface diseases. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ASSOC RESEARCH VISION OPHTHALMOLOGY INC | - |
dc.subject | OCULAR SURFACE | - |
dc.subject | AIR-POLLUTION | - |
dc.subject | AMBIENT LEVELS | - |
dc.subject | MITOCHONDRIAL DAMAGE | - |
dc.subject | APOPTOSIS | - |
dc.subject | ACTIVATION | - |
dc.subject | EXPRESSION | - |
dc.subject | PM2.5 | - |
dc.subject | EYE | - |
dc.subject | EXPOSURE | - |
dc.title | SIRT1 Protects Against Particulate Matter-Induced Oxidative Stress in Human Corneal and Conjunctival Epithelial Cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Song, Jong Suk | - |
dc.identifier.doi | 10.1167/iovs.63.10.19 | - |
dc.identifier.scopusid | 2-s2.0-85139375571 | - |
dc.identifier.wosid | 000876846600004 | - |
dc.identifier.bibliographicCitation | INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, v.63, no.10 | - |
dc.relation.isPartOf | INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE | - |
dc.citation.title | INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE | - |
dc.citation.volume | 63 | - |
dc.citation.number | 10 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Ophthalmology | - |
dc.relation.journalWebOfScienceCategory | Ophthalmology | - |
dc.subject.keywordPlus | OCULAR SURFACE | - |
dc.subject.keywordPlus | AIR-POLLUTION | - |
dc.subject.keywordPlus | AMBIENT LEVELS | - |
dc.subject.keywordPlus | MITOCHONDRIAL DAMAGE | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PM2.5 | - |
dc.subject.keywordPlus | EYE | - |
dc.subject.keywordPlus | EXPOSURE | - |
dc.subject.keywordAuthor | particulate matter | - |
dc.subject.keywordAuthor | corneal/conjunctival epithelial cells | - |
dc.subject.keywordAuthor | oxidative stress | - |
dc.subject.keywordAuthor | reactive oxygen species | - |
dc.subject.keywordAuthor | silent information regulator 1 | - |
dc.subject.keywordAuthor | SRT1720 | - |
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