Mortalin deficiency suppresses fibrosis and induces apoptosis in keloid spheroids
DC Field | Value | Language |
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dc.contributor.author | Lee, Won Jai | - |
dc.contributor.author | Ahn, Hyo Min | - |
dc.contributor.author | Na, Youjin | - |
dc.contributor.author | Wadhwa, Renu | - |
dc.contributor.author | Hong, JinWoo | - |
dc.contributor.author | Yun, Chae-Ok | - |
dc.date.accessioned | 2021-07-30T05:33:11Z | - |
dc.date.available | 2021-07-30T05:33:11Z | - |
dc.date.created | 2021-05-12 | - |
dc.date.issued | 2017-10 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/5377 | - |
dc.description.abstract | Mortalin (Mot) is a mitochondrial chaperone of the heat shock protein 70 family and it's pro-proliferative and anti-apoptosis functions could be associated with keloid pathogenesis, and blocking of mortalin and its interaction with p53 might be a potential novel target for the treatment of keloid. Therefore, we generated mortalin-specific small hairpin (sh) RNAs (dE1-RGD/GFP/shMot) and introduced into keloid spheroids for examination of its apoptotic and anti-fibrotic effect. On keloid tissues, mortalin expression was higher than adjacent normal tissues and it's protein expressions were activated keloid fibroblasts (KFs). After primary keloid spheroid were transduced with dE1-RGD/GFP/shMot for knockdown of mortalin, expression of type I, III collagen, fibronectin, and elastin was significantly reduced and transforming growth factor-beta 1, epidermal growth factor receptor (EGFR), Extracellular Signal-Regulated Kinases 1 and 2 (Erk 1/2), and Smad 2/3 complex protein expression were decreased. In addition, increased TUNEL activities and cytochrome C were observed. Further, for examine of mortalin and p53 interaction, we performed immunofluorescence analysis. Knockdown of mortalin relocated p53 to the cell nucleus in primary keloid spheroids by dE1-RGD/GFP/shMot transduction. These results support the utility of knockdown of mortalin to induce apoptosis and reduce ECMs expression in keloid spheroid, which may be highly beneficial in treating keloids. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Mortalin deficiency suppresses fibrosis and induces apoptosis in keloid spheroids | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Yun, Chae-Ok | - |
dc.identifier.doi | 10.1038/s41598-017-13485-y | - |
dc.identifier.scopusid | 2-s2.0-85031112156 | - |
dc.identifier.wosid | 000412781300025 | - |
dc.identifier.bibliographicCitation | SCIENTIFIC REPORTS, v.7 | - |
dc.relation.isPartOf | SCIENTIFIC REPORTS | - |
dc.citation.title | SCIENTIFIC REPORTS | - |
dc.citation.volume | 7 | - |
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 | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | FIBROBLASTS IN-VITRO | - |
dc.subject.keywordPlus | FUNCTIONAL-CHARACTERIZATION | - |
dc.subject.keywordPlus | TUMOR-GROWTH | - |
dc.subject.keywordPlus | P53 FUNCTION | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | HSP70 | - |
dc.subject.keywordPlus | MORTALIN/MTHSP70/PBP74/GRP75 | - |
dc.subject.keywordPlus | IDENTIFICATION | - |
dc.identifier.url | https://www.nature.com/articles/s41598-017-13485-y | - |
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