Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts
DC Field | Value | Language |
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dc.contributor.author | Park, Seul-Ki | - |
dc.contributor.author | Shin, Ok Sarah | - |
dc.date.accessioned | 2021-09-03T00:21:40Z | - |
dc.date.available | 2021-09-03T00:21:40Z | - |
dc.date.created | 2021-06-19 | - |
dc.date.issued | 2017-10 | - |
dc.identifier.issn | 0906-6705 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/81994 | - |
dc.description.abstract | Metformin is a popular antidiabetic biguanide, which has been considered as a candidate drug for cancer treatment and ageing prevention. Hutchinson-Gilford progeria syndrome (HGPS) is a devastating disease characterized by premature ageing and severe age-associated complications leading to death. The effects of metformin on HGPS dermal fibroblasts remain largely undefined. In this study, we investigated whether metformin could exert a beneficial effect on nuclear abnormalities and delay senescence in fibroblasts derived from HGPS patients. Metformin treatment partially restored normal nuclear phenotypes, delayed senescence, activated the phosphorylation of AMP-activated protein kinase and decreased reactive oxygen species formation in HGPS dermal fibroblasts. Interestingly, metformin reduced the number of phosphorylated histone variant H2AX-positive DNA damage foci and suppressed progerin protein expression, compared to the control. Furthermore, metformin-supplemented aged mice showed higher splenocyte proliferation and mRNA expression of the antioxidant enzyme, superoxide dismutase 2 than the control mice. Collectively, our results show that metformin treatment alleviates the nuclear defects and premature ageing phenotypes in HGPS fibroblasts. Thus, metformin can be considered a promising therapeutic approach for life extension in HGPS. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.subject | SYNDROME MUTATION | - |
dc.subject | IN-VIVO | - |
dc.subject | SENESCENCE | - |
dc.subject | CELLS | - |
dc.subject | ACCUMULATION | - |
dc.subject | PATHWAY | - |
dc.subject | FARNESYLATION | - |
dc.subject | PREVENTS | - |
dc.subject | INSIGHTS | - |
dc.subject | DEFECTS | - |
dc.title | Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Shin, Ok Sarah | - |
dc.identifier.doi | 10.1111/exd.13323 | - |
dc.identifier.scopusid | 2-s2.0-85018972771 | - |
dc.identifier.wosid | 000411801600008 | - |
dc.identifier.bibliographicCitation | EXPERIMENTAL DERMATOLOGY, v.26, no.10, pp.889 - 895 | - |
dc.relation.isPartOf | EXPERIMENTAL DERMATOLOGY | - |
dc.citation.title | EXPERIMENTAL DERMATOLOGY | - |
dc.citation.volume | 26 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | 889 | - |
dc.citation.endPage | 895 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Dermatology | - |
dc.relation.journalWebOfScienceCategory | Dermatology | - |
dc.subject.keywordPlus | SYNDROME MUTATION | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | SENESCENCE | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | ACCUMULATION | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | FARNESYLATION | - |
dc.subject.keywordPlus | PREVENTS | - |
dc.subject.keywordPlus | INSIGHTS | - |
dc.subject.keywordPlus | DEFECTS | - |
dc.subject.keywordAuthor | ageing | - |
dc.subject.keywordAuthor | HGPS | - |
dc.subject.keywordAuthor | metformin | - |
dc.subject.keywordAuthor | progerin | - |
dc.subject.keywordAuthor | senescence | - |
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