• Journal of Plant Biotechnology
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• v.44 no.4
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• pp.409-415
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• 2017

The vegetation period of trees might be prolonged by the delay of the leaf senescence in autumn. Thus, we focused on the generation of senescence-delayed transgenic trees to enhance biomass production. The PagMYC2, a gene containing the basic helix-loop-helix domain, was selected as a candidate for a senescence-delayed transgenic tree. The PagMYC2 gene was specifically induced after treatment with phytohormone jasmonic acid, and upregulated by abiotic stresses such as salinity, osmotic pressure and a low temperature. The constitutive overexpression of the PagMYC2 delayed the leaf senescence and inhibited chlorophyll degradation in the transgenic poplars. Leaf senescence analysis was performed in the leaf tissues of the PagMYC2-over-expression transgenic poplars. The transgenic poplars exhibited higher photochemical efficiency than did a wild type plant under a short-day condition (6 hours light/18 hours darkness) or a low temperature condition ($15^{\circ}C$) that was similar to the weather conditions of autumn. These results suggest that the PagMYC2 is a useful genetic resource to improve biomass production, which is able to sustain growth with senescence-delayed leaves for a long time in autumn.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6191-6196
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• 2012

Aims and Background: Traditional chemotherapy strategies for human leukemia commonly use drugs based on cytotoxicity to eradicate cancer cells. One predicament is that substantial damage to normal tissues is likely to occur in the course of standard treatments. Obviously, it is urgent to explore therapies that can effectively eliminate malignant cells without affecting normal cells. Our previous studies indicated that ginsenoside $Rg_1$ ($Rg_1$), a major active pharmacological ingredient of ginseng, could delay normal hematopoietic stem cell senescence. However, whether $Rg_1$ can induce cancer cell senescence is still unclear. Methods: In the current study, human leukemia K562 cells were subjected to $Rg_1$ exposure. The optimal drug concentration and duration with K562 cells was obtained by MTT colorimetric test. Effects of $Rg_1$ on cell cycle were analyzed using flow cytometry and by SA-${\beta}$-Gal staining. Colony-forming ability was measured by colony-assay. Telomere lengths were assessed by Southern blotting and expression of senescence-associated proteins P21, P16 and RB by Western blotting. Ultrastructural morphology changes were observed by transmission electron microscopy. Results: K562 cells demonstrated a maximum proliferation inhibition rate with an $Rg_1$ concentration of $20{\mu}\;mol{\cdot}L^{-1}$ for 48h, the cells exhibiting dramatic morphological alterations including an enlarged and flat cellular morphology, larger mitochondria and increased number of lysosomes. Senescence associated-${\beta}$-galactosidase (SA-${\beta}$-Gal) activity was increased. K562 cells also had decreased ability for colony formation, and shortened telomere length as well as reduction of proliferating potential and arrestin $G_2$/M phase after $Rg_1$ interaction. The senescence associated proteins P21, P16 and RB were significantly up-regulated. Conclusion: Ginsenoside $Rg_1$ can induce a state of senescence in human leukemia K562 cells, which is associated with p21-Rb and p16-Rb pathways.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.41 no.2
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• pp.135-141
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• 2015

Cell senescence can be identified by cellular changes that occur as a result of intrinsic aging and/or diseases. In case of skin cells, aging and cell senescence caused by external factors results in cessation of cell proliferation and cellular malfunction, which, in turn, accelerates skin aging. In this study, inhibition of cell senescence and enhancement of cell function were studied using cordycepin to evaluate the potential for skin anti-aging agent. By comparing with the number of senescence associated with ${\beta}$-galactosidase (SA-${\beta}$-gal) positive cells in young and replicative aged human fibroblasts, it was found that replicative aged cells showed higher expression of ${\beta}$-galactosidase. Treatment of cordycepin - known as an anti-oxidative and anti-inflammatory agent - reduced ${\beta}$-galactosidase expression in senescent cells and enhanced cell survival in serum-free culture condition. Cordycepin also showed superb inhibition of ROS, which is another indicator of cell senescence. The results of this study proved the anti-aging effect of cordycepin on human fibroblasts and also proposed a possibility of its use as an anti-aging cosmetic ingredient.

• Journal of Ginseng Research
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• v.44 no.2
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• pp.341-349
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• 2020

Background: The replicative senescence of human dermal fibroblasts (HDFs) is accompanied by growth arrest. In our previous study, the treatment of senescent HDFs with Rg3(S) lowered the intrinsic reactive oxygen species (ROS) levels and reversed cellular senescence by inducing peroxiredoxin-3, an antioxidant enzyme. However, the signaling pathways involved in Rg3(S)-induced senescence reversal in HDFs and the relatedness of the stereoisomer Rg3(R) in corresponding signaling pathways are not known yet. Methods: We performed senescence-associated β-galactosidase and cell cycle assays in Rg3(S)-treated senescent HDFs. The levels of ROS, adenosine triphosphate (ATP), and cyclic adenosine monophosphate (cAMP) as well as the mitochondrial DNA copy number, nicotinamide adenine dinucleotide (NAD)⁺/1,4-dihydronicotinamide adenine dinucleotide (NADH) ratio, and NAD-dependent sirtuins expression were measured and compared among young, old, and Rg3(S)-pretreated old HDFs. Major signaling pathways of phosphatidylinositol 3-kinase/Akt, 5' adenosine monophosphate-activated protein kinase (AMPK), and sirtuin 1/3, including cell cycle regulatory proteins, were examined by immunoblot analysis. Results: Ginsenoside Rg3(S) reversed the replicative senescence of HDFs by restoring the ATP level and NAD⁺/NADH ratio in downregulated senescent HDFs. Rg3(S) recovered directly the cellular levels of ROS and the NAD⁺/NADH ratio in young HDFs inactivated by rotenone. Rg3(S) mainly downregulated phosphatidylinositol 3-kinase/Akt through the inhibition of mTOR by cell cycle regulators like p53/p21 in senescent HDFs, whereas Rg3(R) did not alter the corresponding signaling pathways. Rg3(S)-activated sirtuin 3/PGC1α to stimulate mitochondrial biogenesis. Conclusion: Cellular molecular analysis suggests that Rg3(S) specifically reverses the replicative senescence of HDFs by modulating Akt-mTOR-sirtuin signaling to promote the biogenesis of mitochondria.

• Proceedings of the Korean Society of Crop Science Conference
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• 2017.10a
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• pp.238-238
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• 2017

• Proceedings of the Korean Society of Life Science Conference
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• 2008.10a
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• pp.38.1-38.1
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• 2008

• Proceedings of the Korean Society of Embryo Transfer Conference
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• 2006.10a
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• pp.62-62
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• 2006

• Proceedings of the Botanical Society of Korea Conference
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• 2001.04a
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• pp.5-5
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• 2001

• Proceedings of the Botanical Society of Korea Conference
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• 2002.04a
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• pp.98-98
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• 2002

• International Journal of Oral Biology
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• v.32 no.1
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• pp.35-43
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• 2007

Tooth loss in elderly is mainly caused by alveolar bone loss via severe periodontitis. Although the severity of periodontitis is known to be affected by age, the aging process or the genetic changes during the aging of periodontal tissue cells are not well characterized. In this study, we investigated the effect of in vitro aging on the change of gene expression pattern in periodontal fibroblasts. Gingival fibroblasts (GF) and periodontal ligament fibroblasts (PDL) were obtained from two young patients and replicative senescence was induced by sequential subcultivation. When more than 90% cells were positively stained with senescence-associated ${\beta},-galactosidase$, those cells were regarded as aged cells. In aged GF and PDL, the level of phosphorylated retinoblastoma (RB) and $p16^{INK4A}$ protein was significantly decreased and increased, respectively. However, the protein level of p53 and p21, well known senescence-inducing genes, did not increase in aged GF and PDL. Although $p27^{Kip1}$ and $p15^{INK4B}$, another cyclin-dependent kinase inhibitors, were reported to be involved in replicative senescence of human cells, they were decreased in aged GF and PDL. Because senescent cells showed flattened and enlarged cell shape and are known to have increased focal adhesion, we examined the protein level of several integrins. Aged GF and PDL showed increased protein level of integrin ${\alpha}2$, ${\alpha}v$, and ${\beta}1$. When the gene expression profiles of actively proliferating young cells and aged cells were compared by cDNA microarray of 3,063 genes and were confirmed by reverse transcription-polymerase chain reaction, 7 genes and 15 genes were significantly and commonly increased and decreased, respectively, in aged GF and PDL. Among them, included are the genes that were known to be involved in the regulation of cell cycle, gene transcription, or integrin signaling. The change of gene expression pattern in GF and PDL was minimally similar to that of oral keratinocyte. These results suggest that $p16^{INK4A}/RB$ might be involved in replicative senescence of periodontal fibroblasts and the change of gene expression profile during aging process is cell type specific.