Proteomic and metabolomic analysis of H2O2-induced premature senescent human mesenchymal stem cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Ji-Soo | - |
dc.contributor.author | Kim, Eui-Jin | - |
dc.contributor.author | Kim, Hyun-Jung | - |
dc.contributor.author | Yang, Ji-Young | - |
dc.contributor.author | Hwang, Geum-Sook | - |
dc.contributor.author | Kim, Chan-Wha | - |
dc.date.accessioned | 2021-09-07T12:02:48Z | - |
dc.date.available | 2021-09-07T12:02:48Z | - |
dc.date.created | 2021-06-14 | - |
dc.date.issued | 2011-06 | - |
dc.identifier.issn | 0531-5565 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/112342 | - |
dc.description.abstract | Stress induced premature senescence (SIPS) occurs after exposure to many different sublethal stresses including H2O2, hyperoxia, or tert-butylhydroperoxide. Human mesenchymal stem cells (hMSCs) exhibit limited proliferative potential in vitro, the so-called Hayflick limit. According to the free-radical theory, reactive oxygen species (ROS) might be the candidates responsible for senescence and age-related diseases. H2O2 may be responsible for the production of high levels of ROS, in which the redox balance is disturbed and the cells shift into a state of oxidative stress, which subsequently leads to premature senescence with shortening telomeres. H2O2 has been the most commonly used inducer of SIPS, which shares features of replicative senescence (RS) including a similar morphology, senescence-associated beta-galactosidase activity, cell cycle regulation, etc. Therefore, in this study, the senescence of hMSC during SIPS was confirmed using a range of different analytical methods. In addition, we determined five differentially expressed spots in the 2-DE map, which were identified as Annexin A2 (ANKA2), myosin light chain 2 (MLC2), peroxisomal enoyl-CoA hydratase 1 (ECH1), prosomal protein P30-33K (PSMA1) and mutant beta-actin by ESI-Q-TOF MS/MS. Also, proton (H-1) nuclear magnetic resonance spectroscopy (NMR) was used to elucidate the difference between metabolites in the control and hMSCs treated with H2O2. Among these metabolites, choline and leucine were identified by H-1-NMR as up-regulated metabolites and glycine and proline were identified as down-regulated metabolites. (C) 2011 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | - |
dc.subject | PROTEASOME INHIBITION | - |
dc.subject | CELLULAR SENESCENCE | - |
dc.subject | PROLINE OXIDASE | - |
dc.subject | PHOSPHATIDYLCHOLINE BIOSYNTHESIS | - |
dc.subject | PROTEIN-DEGRADATION | - |
dc.subject | SIGNAL-TRANSDUCTION | - |
dc.subject | P53-INDUCED GENE-6 | - |
dc.subject | OXIDIZED PROTEINS | - |
dc.subject | HUMAN FIBROBLASTS | - |
dc.subject | CHOLINE KINASE | - |
dc.title | Proteomic and metabolomic analysis of H2O2-induced premature senescent human mesenchymal stem cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Chan-Wha | - |
dc.identifier.doi | 10.1016/j.exger.2011.02.012 | - |
dc.identifier.scopusid | 2-s2.0-79955613626 | - |
dc.identifier.wosid | 000291337200011 | - |
dc.identifier.bibliographicCitation | EXPERIMENTAL GERONTOLOGY, v.46, no.6, pp.500 - 510 | - |
dc.relation.isPartOf | EXPERIMENTAL GERONTOLOGY | - |
dc.citation.title | EXPERIMENTAL GERONTOLOGY | - |
dc.citation.volume | 46 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 500 | - |
dc.citation.endPage | 510 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Geriatrics & Gerontology | - |
dc.relation.journalWebOfScienceCategory | Geriatrics & Gerontology | - |
dc.subject.keywordPlus | PROTEASOME INHIBITION | - |
dc.subject.keywordPlus | CELLULAR SENESCENCE | - |
dc.subject.keywordPlus | PROLINE OXIDASE | - |
dc.subject.keywordPlus | PHOSPHATIDYLCHOLINE BIOSYNTHESIS | - |
dc.subject.keywordPlus | PROTEIN-DEGRADATION | - |
dc.subject.keywordPlus | SIGNAL-TRANSDUCTION | - |
dc.subject.keywordPlus | P53-INDUCED GENE-6 | - |
dc.subject.keywordPlus | OXIDIZED PROTEINS | - |
dc.subject.keywordPlus | HUMAN FIBROBLASTS | - |
dc.subject.keywordPlus | CHOLINE KINASE | - |
dc.subject.keywordAuthor | Cellular senescence | - |
dc.subject.keywordAuthor | Mesenchymal stem cells | - |
dc.subject.keywordAuthor | Reactive oxygen species | - |
dc.subject.keywordAuthor | Proteomics | - |
dc.subject.keywordAuthor | Metabolomics | - |
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.