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 β-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 (ANXA2), myosin light chain 2 (MLC2), peroxisomal enoyl-CoA hydratase 1 (ECH1), prosomal protein P30-33K (PSMA1) and mutant β-actin by ESI-Q-TOF MS/MS. Also, proton (1H) 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 1H-NMR as up-regulated metabolites and glycine and proline were identified as down-regulated metabolites.
| Original language | English |
|---|---|
| Pages (from-to) | 500-510 |
| Number of pages | 11 |
| Journal | Experimental Gerontology |
| Volume | 46 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2011 Jun 1 |
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Keywords
- Cellular senescence
- Mesenchymal stem cells
- Metabolomics
- Proteomics
- Reactive oxygen species
ASJC Scopus subject areas
- Ageing
- Biochemistry
- Cell Biology
- Endocrinology
- Genetics
- Molecular Biology
Cite this
Proteomic and metabolomic analysis of H2O2-induced premature senescent human mesenchymal stem cells. / Kim, Ji Soo; Kim, Eui Jin; Kim, Hyun Jung; Yang, Ji Young; Hwang, Geum Sook; Kim, Chan Wha.
In: Experimental Gerontology, Vol. 46, No. 6, 01.06.2011, p. 500-510.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Proteomic and metabolomic analysis of H2O2-induced premature senescent human mesenchymal stem cells
AU - Kim, Ji Soo
AU - Kim, Eui Jin
AU - Kim, Hyun Jung
AU - Yang, Ji Young
AU - Hwang, Geum Sook
AU - Kim, Chan Wha
PY - 2011/6/1
Y1 - 2011/6/1
N2 - 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 β-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 (ANXA2), myosin light chain 2 (MLC2), peroxisomal enoyl-CoA hydratase 1 (ECH1), prosomal protein P30-33K (PSMA1) and mutant β-actin by ESI-Q-TOF MS/MS. Also, proton (1H) 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 1H-NMR as up-regulated metabolites and glycine and proline were identified as down-regulated metabolites.
AB - 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 β-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 (ANXA2), myosin light chain 2 (MLC2), peroxisomal enoyl-CoA hydratase 1 (ECH1), prosomal protein P30-33K (PSMA1) and mutant β-actin by ESI-Q-TOF MS/MS. Also, proton (1H) 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 1H-NMR as up-regulated metabolites and glycine and proline were identified as down-regulated metabolites.
KW - Cellular senescence
KW - Mesenchymal stem cells
KW - Metabolomics
KW - Proteomics
KW - Reactive oxygen species
UR - http://www.scopus.com/inward/record.url?scp=79955613626&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79955613626&partnerID=8YFLogxK
U2 - 10.1016/j.exger.2011.02.012
DO - 10.1016/j.exger.2011.02.012
M3 - Article
C2 - 21382465
AN - SCOPUS:79955613626
VL - 46
SP - 500
EP - 510
JO - Experimental Gerontology
JF - Experimental Gerontology
SN - 0531-5565
IS - 6
ER -