• BMB Reports
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• v.51 no.7
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• pp.317-318
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• 2018

Plants are unable to relocate themselves to a more favorable location and thus have to deal with developmental programs and environmental cues wherever they happen to be. It is yet largely unknown how plant cells coordinate cellular activities and architectures to accomplish developmental processes and respond to environmental changes. By identifying and establishing a new cellular model system, we have discovered that two neighboring cell types in the abscission zone (AZ) of Arabidopsis flowers coordinate their activities to ensure a precise "cut" through a highly restricted area of plant tissue to bring about organ separation. From this perspective, we further discuss the essence of cellular coordination in AZ, the key molecules controlling the organ separation, and relevant implications.

• Korean Journal of Medicinal Crop Science
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• v.21 no.1
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• pp.1-6
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• 2013

Buckwheat (Fagopyrum esculentum) has been known for having strong anti-oxidant, anti-mutagenic, and anti-carcinogenic activities. The free radical theory of aging, also known as the oxidative stress theory of aging, claims that cellular oxidative damage accumulated with time is a major causal factor of aging. In the present study, we investigated the effect of buckwheat extracts on resistance to oxidative stress and aging using Caenorhabditis elegans as a model system. Survival under an oxidative-stress condition induced by paraquat increased markedly following 500mg/L buckwheat extracts treatment, suggesting lower cellular oxidative damage by buckwheat extracts. A lifespan assay also revealed that treatment of buckwheat extracts significantly extended both the mean and maximum lifespan in C. elegans. Interestingly, this lifespan-extension by buckwheat extracts was not accompanied by reduced fertility. These findings suggest that buckwheat extracts can confer longevity phenotype to C. elegans through its strong anti-oxidant activity and support the aging theory which emphasizes a pivotal role of oxidative stress during aging.

• BMB Reports
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• v.52 no.1
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• pp.24-34
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• 2019

Sirtuin is an essential factor that delays cellular senescence and extends the organismal lifespan through the regulation of diverse cellular processes. Suppression of cellular senescence by Sirtuin is mainly mediated through delaying the age-related telomere attrition, sustaining genome integrity and promotion of DNA damage repair. In addition, Sirtuin modulates the organismal lifespan by interacting with several lifespan regulating signaling pathways including insulin/IGF-1 signaling pathway, AMP-activated protein kinase, and forkhead box O. Although still controversial, it is suggested that the prolongevity effect of Sirtuin is dependent with the level of and with the tissue expression of Sirtuin. Since Sirtuin is also believed to mediate the prolongevity effect of calorie restriction, activators of Sirtuin have attracted the attention of researchers to develop therapeutics for age-related diseases. Resveratrol, a phytochemical rich in the skin of red grapes and wine, has been actively investigated to activate Sirtuin activity with consequent beneficial effects on aging. This article reviews the evidences and controversies regarding the roles of Sirtuin on cellular senescence and lifespan extension, and summarizes the activators of Sirtuin including Sirtuin-activating compounds and compounds that increase the cellular level of nicotinamide dinucleotide.

• Journal of Yeungnam Medical Science
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• v.34 no.1
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• pp.1-10
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• 2017

The life history of man is summarized as a birth-aging-disease-death. Man eventually ages and dies. How long can humans live? What is aging? Why do we age? Is aging inevitable? Can we rejuvenate? Recent researches on biological aging suggest that humans might overcome aging and rejuvenate. In this paper, we review the biologic characteristics of aging and the latest results of biological aging research, implicating that aging can be controlled, further treated, and that humans can ultimately be rejuvenated.

• Proceedings of the SCSK Conference
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• 2003.09a
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• pp.291-312
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• 2003

Reactive oxygen species are capable of damaging biomolecules such as lipids, proteins, and DNA, which can not only lead to various diseases, but also oxidative damage resulting aging. In our previous study, Cercis chinensis (Leguminosae) showed a potent antioxidant activity. Nineteen compounds were isolated through antioxidant activity-guided fractionation. The C. chinensis extract and some of the constituents exhibited a potent antioxidant activity on the free radicals and lipid peroxidation and a notable protective effect on the t-BuOOH induced oxidative damage. In vivo test of skin damage induced by UVB irradiation, the extract of C. chinensis and a constituent, piceatannol, exhibited a significant protective effect. The life-span of the HEK-N/F cells were extended by 1.21-2.12 fold as a result of the continuous administration of 3 $\mu\textrm{g}$/ml of the C. chinensis extract and the active constituents compared to that of the control. These observations were attributed to the inhibitory effect of the C. chinensis extract and its constituents on the age-dependent shortening of the telomere. Thus, C. chinensis was demonstrated to protect the skin cells against oxidative stress and inhibit thereby the cellular aging, followed by expectation as anti-aging cosmetic ingredient.

• Journal of dental hygiene science
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• v.22 no.3
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• pp.164-170
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• 2022

Background: When cells are damaged by nicotine, cellular senescence due to oxidative stress accelerates. In addition, stress-induced inflammatory response and cellular senescence cause the accumulation of damaged organelles in cells, and autophagy appears to remove them. Conversely, when autophagy is reduced, harmful cell components accumulate, and aging is accelerated. This study aimed to determine the association between nicotine-induced cellular senescence and autophagy expression patterns in human gingival fibroblasts. Methods: Cells were treated with various concentrations of nicotine (0, 0.1, 0.5, 1, 2, and 5 mM) and 10 nM rapamycin was added to 1 mM nicotine to investigate the relationship between autophagy and cellular senescence. Cell viability was confirmed using WST-8 and the degree of cellular senescence was measured by SA-β-gal staining. The expression of the inflammatory proteins (COX-2 and iNOS) and autophagy markers (LC3-II, p62, and Beclin-1) was analyzed by western blotting. Results: The cell viability tended to decrease in a concentration-dependent manner. COX-2 showed no concentration-dependent expression and iNOS increased in the 0.5 mM nicotine treated group. The degree of cellular senescence was the highest in the 1 mM nicotine treatment group. In the group treated with rapamycin and nicotine, the conversion ratio of LC3-II to LC3-I was the highest, that of p62 was the lowest, and the level of Beclin-1 proteins was significantly increased. Furthermore, the degree of cellular senescence was reduced in the group in which rapamycin was added to nicotine compared to that in the group treated with nicotine alone. Conclusion: This study provides evidence that autophagy activated in an aging environment reduces cellular senescence to a certain some extent.

• Biomolecules & Therapeutics
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• v.32 no.2
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• pp.171-182
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• 2024

All cells are equipped with intricate signaling networks to meet the energy demands and respond to the nutrient availability in the body. AMP-activated protein kinase (AMPK) is among the most potent regulators of cellular energy balance. Under ATP -deprived conditions, AMPK phosphorylates substrates and affects various biological processes, such as lipid/glucose metabolism and protein synthesis. These actions further affect the cell growth, death, and functions, altering the cellular outcomes in energy-restricted environments. AMPK plays vital roles in maintaining good health. AMPK dysfunction is observed in various chronic diseases, making it a promising target for preventing and alleviating such diseases. Herein, we highlight the different AMPK functions, especially in allergy, aging, and cancer, to facilitate the development of new therapeutic approaches in the future.

• BMB Reports
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• v.53 no.9
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• pp.458-465
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• 2020

Metastasis is the main culprit of the great majority of cancerrelated deaths. However, the complicated process of the invasion-metastasis cascade remains the least understood aspect of cancer biology. Telomerase plays a pivotal role in bypassing cellular senescence and sustaining the cancer progression by maintaining telomere homeostasis and genomic integrity. Telomerase reverse transcriptase (TERT) exerts a series of fundamental functions that are independent of its enzymatic cellular activity, including proliferation, inflammation, epithelia-mesenchymal transition (EMT), angiogenesis, DNA repair, and gene expression. Accumulating evidence indicates that TERT may facilitate most steps of the invasion-metastasis cascade. In this review, we summarize important advances that have revealed some of the mechanisms by which TERT facilitates tumor metastasis, providing an update on the non-canonical functions of telomerase beyond telomere maintaining.

• Genomics & Informatics
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• v.14 no.1
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• pp.2-11
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• 2016

The advances in mass spectrometry-based proteomics technologies have enabled the generation of global proteome data from tissue or body fluid samples collected from a broad spectrum of human diseases. Comparative proteomic analysis of global proteome data identifies and prioritizes the proteins showing altered abundances, called differentially expressed proteins (DEPs), in disease samples, compared to control samples. Protein biomarker candidates that can serve as indicators of disease states are then selected as key molecules among these proteins. Recently, it has been addressed that cellular pathways can provide better indications of disease states than individual molecules and also network analysis of the DEPs enables effective identification of cellular pathways altered in disease conditions and key molecules representing the altered cellular pathways. Accordingly, a number of network-based approaches to identify disease-related pathways and representative molecules of such pathways have been developed. In this review, we summarize analytical platforms for network-based protein biomarker discovery and key components in the platforms.

• Journal of Life Science
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• v.34 no.1
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• pp.68-77
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• 2024

Airborne particulate matter (PM) is an environmentally hazardous pollutant that originates from various sources. PM is comprised of solid particles and liquid droplets of diverse composition and size. Hazardous chemical compositions of PM include elemental and organic carbon, organic compounds, biological compounds and metals. Upon acute and chronic PM exposure, toxic contaminants enter and accumulate within physiological systems and prompt cell structure changes accompanied with intracellular endoplasmic reticulum stress, mitochondrial dysfunction, oxidative stress, inflammation, lipid accumulation, and cell cycle arrest. Ultimately, these cellular response leads to the development of key characteristics of aging. In addition, PM internalization enhances autophagy reflux and lysosomal dysfunction, which is involved in cell aging. Previous studies have emphasized a positive association between PM and increased mortality or decreased lifespan, although these are evidenced mostly by observational studies. Direct evidence of the link between PM and aging is still limited. This review evaluates the evidence from not only observational studies but also in vitro and in vivo evidence of PM on aging progression and age-related diseases development. This evidence is based on age-associated cellular changes including endoplasmic reticulum stress, mitochondrial dysfunction, oxidative stress, inflammation, adipose accumulation, autophagy, which strengthen the association between PM exposure and aging. Understanding the underlying cellular responses under PM may allow for the development of new therapeutic targets for PM-induced aging.