The Antisenescence Effect of <i>Trans</i>-Cinnamaldehyde on Adipose-Derived Stem Cells

Rajamani, Karthyayani; Lin, Yi‐Chun; Wen, Tung-Chou; Hsieh, Jeanne; Subeq, Yi‐Maun; Liu, Jen‐Wei; Lin, Po Ting; Harn, Horng‐Jyh; Lin, Shinn‐Zong; Chiou, Tzyy‐Wen

doi:10.3727/096368915x686959

Cited by 11 publications

(10 citation statements)

References 38 publications

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“…These observations were all corroborated by results obtained from our analysis of SA β-Gal activity after 24, 48 and 72 h from the end of the H 2 O 2 treatment, where both hASCs and hWJ-MSCs showed an increase of the SA β-Gal activity. In particular, the higher senescent effect was evident at 48 h. A similar trend was seen in other researches, although it was obtained at different experimental times 42 - 44 .…”

Section: Discussionsupporting

confidence: 89%

“…Here, we found that in both cell populations, H 2 O 2 not only inhibited cell proliferation in a dose-dependent fashion, but it also affected the persistence of the anti-proliferative effect after the end of exposure (up to 48 or 72 h) in a manner that was dependent upon the duration (1 or 2 h) of the treatment itself. These results are coherent with the reduction of cell vitality observed in hWJ-MSCs 43 - 45 and hASCs 39 , 42 treated with higher concentrations of H 2 O 2 (until 2000 μM) but at low subcultured passages. We also observed a growth slowdown of cells treated with H 2 O 2 400 μM, and a cell inability to re-plate.…”

Section: Discussionsupporting

confidence: 83%

“…It has been recently shown that SOD2 overexpression in ASCs promotes cell resistance to oxidative stress 40 . Moreover, H 2 O 2 treatment provokes DNA breaks 41 , raises SA β-Gal positive cells 42 , alters the expression of senescent marker genes, as well as p53 , p21 , mitogen-activated protein kinase 14 ( MAPK14 , alias p38 ) and sirtuin 1 ( SIRT1 ) 38 , 39 , 42 , and increases apoptosis with a decline of pro-survival gene expression 38 . It has been recently shown that also human Wharton's Jelly-derived MSCs (hWJ-MSCs) treated with H 2 O 2 undergo premature senescence at early culture passages: these cells show typical changes in morphology 43 , slow their proliferation 44 , 45 , result positive for SA β-Gal 43 , 44 , express typical senescence 43 and pro-apoptotic gene markers, while displaying a down-regulation of survival genes 44 , 46 .…”

Section: Introductionmentioning

confidence: 99%

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Comparison of Oxidative Stress Effects on Senescence Patterning of Human Adult and Perinatal Tissue-Derived Stem Cells in Short and Long-term Cultures

et al. 2018

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Human Mesenchymal Stem Cells (hMSCs) undergo senescence in lifespan. In most clinical trials, hMSCs experience long-term expansion ex vivo to increase cell number prior to transplantation, which unfortunately leads to cell senescence, hampering post-transplant outcomes.Hydrogen peroxide (H2O2) in vitro represents a rapid, time and cost-effective tool, commonly used as oxidative stress tantalizing the stem cell ability to cope with a hostile environment, recapitulating the onset and progression of cellular senescence.Here, H2O2 at different concentrations (ranging from 50 to 400 μM) and time exposures (1 or 2 hours - h), was used for the first time to compare the behavior of human Adipose tissue-derived Stem Cells (hASCs) and human Wharton's Jelly-derived MSCs (hWJ-MSCs), as representative of adult and perinatal tissue-derived stem cells, respectively. We showed timely different responses of hASCs and hWJ-MSCs at low and high subculture passages, concerning the cell proliferation, the cell senescence-associated β-Galactosidase activity, the capability of these cells to undergo passages, the morphological changes and the gene expression of tumor protein p53 (TP53, alias p53) and cyclin dependent kinase inhibitor 1A (CDKN1A, alias p21) post H2O2 treatments.The comparison between the hASC and hWJ-MSC response to oxidative stress induced by H2O2 is a useful tool to assess the biological mechanisms at the basis of hMSC senescence, but it could also provide two models amenable to test in vitro putative anti-senescence modulators and develop anti-senescence strategies.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

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Comparison of Oxidative Stress Effects on Senescence Patterning of Human Adult and Perinatal Tissue-Derived Stem Cells in Short and Long-term Cultures

et al. 2018

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“…Human telomerase reverse transcriptase (hTERT) is a catalytic subunit of human telomerase (13,14), which provides the reverse transcriptase activity needed to maintain the length of the telomere (15). It has been shown that overexpression of hTERT increases the cell lifespan of ameloblastoma cells (16), human fibroblasts (17), adipose-derived stem cells (18) and endothelial cells (19) in vitro. Several studies have demonstrated that the modification of human MSCs with the hTERT gene generates cells with an improved ability for proliferation and cell renewal that retain their potential to differentiate into osteocytes, adipocytes, chondrocytes and gingival epithelial cell lines (20)(21)(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

Expression of human telomerase reverse transcriptase mediates the senescence of mesenchymal stem cells through the PI3K/AKT signaling pathway

Zhao

Wang

et al. 2015

International Journal of Molecular Medicine

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Multipotent mesenchymal stem cells (MSCs) are widely used as seed cells in studies of tissue engineering and regenerative medicine; however, their clinical application is limited due to replicative senescence. It has been demonstrated that telomerase expression extends the lifespan and maintains the bone-forming ability of MSCs; however, the detailed role and the underlying molecular mechanisms in MSCs remain largely unknown. In the present study, we found that senescence was associated with human telomerase reverse transcriptase (hTERT) expression, and telomere length and telomerase activity. We established a short interfering RNA (siRNA) targeting hTERT and a gene expression vector carrying hTERT and transfected these into the MSCs to investigate the detailed role and the underlying molecular mechanisms of action of hTERT in MSCs. We found that the downregulation of hTERT by siRNA markedly decreased telomere length and telomerase activity in the MSCs, whereas the overexpression of hTERT increased telomere length and telomerase activity in the MSCs. The downregulation of hTERT inhibited cell proliferation and promoted the senescence and apoptosis of MSCs, whereas the upregulation of hTERT increased cell proliferation and decreased the senescence and apoptosis of MSCs. Of note, we also found that the activation of the PI3K/AKT signaling pathway was mediated by hTERT and that blocking this pathway using LY294002 inhibited hTERT expression, induced senescence and decreased the proliferation of MSCs. These findings reveal a previously unknown regulatory mechanism of hTERT, indicating that hTERT mediates the senescence of MSCs through the PI3K/AKT signaling pathway.

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“…Cells were seeded in the Lab-Tek II Chamber Slide System of 8-well plates (Nunc) at 3 × 10 4 cells/well. After 24 h, cells were treated with H 2 O 2 (50,100,150,200 and 400 µM) for 1h. To evaluate senescence, the Galactosidase Detection Kit (Abcam, Cambridge, UK) was used after the end of H 2 O 2 treatment (at 24, 48, or 72 h) according to the fabricator's instructions.…”

Section: Senescence-associated β-Galactosidase Assaymentioning

confidence: 99%

Role of Oxidative Stress in the Senescence Pattern of Auditory Cells in Age-Related Hearing Loss

et al. 2021

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Age-related hearing loss (ARHL) is an increasing and gradual sensorineural hearing dysfunction. Oxidative stress is an essential factor in developing ARHL; additionally, premature senescence of auditory cells induced by oxidative stress can produce hearing loss. Hydrogen peroxide (H2O2) represents a method commonly used to generate cellular senescence in vitro. The objective of the present paper is to study H2O2-induced senescence patterns in three auditory cell lines (House Ear Institute-Organ of Corti 1, HEI-OC1; organ of Corti, OC-k3, and stria vascularis, SV-k1 cells) to elucidate the intrinsic mechanisms responsible for ARHL. The auditory cells were exposed to H2O2 at different concentrations and times. The results obtained show different responses of the hearing cells concerning cell growth, β-galactosidase activity, morphological changes, mitochondrial activation, levels of oxidative stress, and other markers of cell damage (Forkhead box O3a, FoxO3a, and 8-oxoguanine, 8-oxoG). Comparison between the responses of these auditory cells to H2O2 is a helpful method to evaluate the molecular mechanisms responsible for these auditory cells’ senescence. Furthermore, this in vitro model could help develop anti-senescent therapeutic strategies for the treatment of AHRL.

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The Antisenescence Effect of Trans-Cinnamaldehyde on Adipose-Derived Stem Cells

Cited by 11 publications

References 38 publications

Comparison of Oxidative Stress Effects on Senescence Patterning of Human Adult and Perinatal Tissue-Derived Stem Cells in Short and Long-term Cultures

Comparison of Oxidative Stress Effects on Senescence Patterning of Human Adult and Perinatal Tissue-Derived Stem Cells in Short and Long-term Cultures

Expression of human telomerase reverse transcriptase mediates the senescence of mesenchymal stem cells through the PI3K/AKT signaling pathway

Role of Oxidative Stress in the Senescence Pattern of Auditory Cells in Age-Related Hearing Loss

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