• Osteoporosis and Sarcopenia
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• 제3권3호
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• pp.117-122
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• 2017

Sarcopenia is the degenerative loss of muscle mass and function with aging. Recently sarcopenia was recognized as a clinical disease by the International Classification of Disease, 10th revision, Clinical Modification. An imbalance between protein synthesis and degradation causes a gradual loss of muscle mass, resulting in a decline of muscle function as a progress of sarcopenia. Many mechanisms involved in the onset of sarcopenia include age-related factors as well as activity-, disease-, and nutrition-related factors. The stage of sarcopenia reflecting the severity of conditions assists clinical management of sarcopenia. It is important that systemic descriptions of the disease conditions include age, sex, and other environmental risk factors as well as levels of physical function. To develop a new therapeutic intervention needed is the detailed understanding of molecular and cellular mechanisms by which apoptosis, autophagy, atrophy, and hypertrophy occur in the muscle stem cells, myotubes, and/or neuromuscular junction. The new strategy to managing sarcopenia will be signal-modulating small molecules, natural compounds, repurposing of old drugs, and muscle-specific microRNAs.

• Journal of Nutrition and Health
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• 제24권5호
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• pp.431-441
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• 1991

To investigate the influence of age and dietary fat level on the immune function and the growing potential of the fibroblast cells, male rats of 2 month, 6 month and 30 month of age were fed either 6% or 30% fat diet for 16 weeks. The weight of thymus decreased linearly with increasing age. And this age-dependent degeneration of thymus was delayed in rats fed low fat diets. The blastogenesis of spleen lymphocytes to PHA, ConA, and PWM was decreased with increasing age, however, no effect of dietary fat level was observed. The age-related decline in ratios of PHA/ConA response may suggest that T suppressor cell activity increases with age. In cell culture system, lung fibroblast cells from 30M rats showed lower plating efficiency. longer doubling time. and shorter cumulative doubling potential than those from 2M or 6M animals. Also. the morphology of fibroblasts from 30M rats was tended to be rouned rather than flattened and more variable in size and being generally larger. wherease those from 2M and 6M rats were uniform in size and adhered tightly to the culture vessel in ordered arrays. Therefore fibroblast cell culture system tried in this study reflects the changes of cellular aging.

• IMMUNE NETWORK
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• 제16권3호
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• pp.183-188
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• 2016

Sirtuin family members with lysine deacetylase activity are known to play an important role in anti-aging and longevity. Cellular senescence is one of the hallmarks of aging, and downregulation of sirtuin is reported to induce premature senescence. In this study, we investigated the effects of small-molecule sirtuin inhibitors on cellular senescence. Various small molecules such as tenovin-1 and EX527 were employed for direct sirtuin activity inhibition. U251, SNB-75, and U87MG glioblastoma cells treated with sirtuin inhibitors exhibited phenotypes with nuclear enlargement. Furthermore, treatment of rat primary astrocytes with tenovin-1 also increased the size of the nucleus. The activity of senescence-associated β-galactosidase, a marker of cellular senescence, was induced by tenovin-1 and EX527 treatment in U87MG glioblastoma cells. Consistent with the senescent phenotype, treatment with tenovin-1 increased p53 expression in U87MG cells. This study demonstrated the senescence-inducing effect of sirtuin inhibitors, which are potentially useful tools for senescence research.

• IMMUNE NETWORK
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• 제16권5호
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• pp.286-295
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• 2016

Cellular replicative senescence is a major contributing factor to aging and to the development and progression of aging-associated diseases. In this study, we sought to determine viral replication efficiency of influenza virus (IFV) and Varicella Zoster Virus (VZV) infection in senescent cells. Primary human bronchial epithelial cells (HBE) or human dermal fibroblasts (HDF) were allowed to undergo numbers of passages to induce replicative senescence. Induction of replicative senescence in cells was validated by positive senescence-associated b-galactosidase staining. Increased susceptibility to both IFV and VZV infection was observed in senescent HBE and HDF cells, respectively, resulting in higher numbers of plaque formation, along with the upregulation of major viral antigen expression than that in the non-senescent cells. Interestingly, mRNA fold induction level of virus-induced type I interferon (IFN) was attenuated by senescence, whereas IFN-mediated antiviral effect remained robust and potent in virus-infected senescent cells. Additionally, we show that a longevity-promoting gene, sirtuin 1 (SIRT1), has antiviral role against influenza virus infection. In conclusion, our data indicate that enhanced viral replication by cellular senescence could be due to senescence-mediated reduction of virus-induced type I IFN expression.

• Molecules and Cells
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• 제42권3호
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• pp.210-217
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• 2019

The maintenance of mitochondrial function is closely linked to the control of senescence. In our previous study, we uncovered a novel mechanism in which senescence amelioration in normal aging cells is mediated by the recovered mitochondrial function upon Ataxia telangiectasia mutated (ATM) inhibition. However, it remains elusive whether this mechanism is also applicable to senescence amelioration in accelerated aging cells. In this study, we examined the role of ATM inhibition on mitochondrial function in Hutchinson-Gilford progeria syndrome (HGPS) and Werner syndrome (WS) cells. We found that ATM inhibition induced mitochondrial functional recovery accompanied by metabolic reprogramming, which has been known to be a prerequisite for senescence alleviation in normal aging cells. Indeed, the induced mitochondrial metabolic reprogramming was coupled with senescence amelioration in accelerated aging cells. Furthermore, the therapeutic effect via ATM inhibition was observed in HGPS as evidenced by reduced progerin accumulation with concomitant decrease of abnormal nuclear morphology. Taken together, our data indicate that the mitochondrial functional recovery by ATM inhibition might represent a promising strategy to ameliorate the accelerated aging phenotypes and to treat age-related disease.

• 한방안이비인후피부과학회지
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• 제17권1호
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• pp.16-33
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• 2004

In Oriental medicine, aging is just a natural process like change of seasons. Ancient Oriental people accepted it as a natural thing to be growing older and to die at last. The science of aging has advanced dramatically. In the last 2 decades, advances in genetics and molecular biology have led to extraordinary new understandings in how cells age, how apoptosis programs cells to die, and how neuroendocrinology plays a role in the lifespan of organisms. Today, the matter of primary concern about aging is a cellular and mitochondrial damage of human body induced by reactive oxygen species(ROS). The skin aging can be divided into two areas, intrinsic(chronologic)-aging and photo-aging. There are lots of photo damage about skin aging. The skin is increasingly exposed to ultraviolet(UV) irradiation in life. Therefore, the risk of photo-oxidative damage of the skin induced by reactive oxygen species(ROS) has increased substantially. Nowadays, many people believe that they can stop or at least delay the process of aging. There are lots of treatments that promise to slow the process of aging and the associated ailments. Many of these treatments, for example, exercise, Vit E, Vit C therapy, hormone therapy, restrict diet, are gradually being subjected to clinical trials. But in spite of all efforts, researches and investigations, there is no single method or treatment which is revealed to be truly effective for delaying progress of aging. Every methods insisted on effect for delaying aging process, has its dark side. All we can do is just keeping ourself healthy until the time of death.

• Reproductive and Developmental Biology
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• 제36권1호
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• pp.55-64
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• 2012

Peroxiredoxin II (Prdx II; a typical 2-Cys Prdx) has been originally isolated from erythrocytes, and its structure and peroxidase activity have been adequately studied. Prdx II has been reported to protect a wide range of cellular environments as antioxidant enzyme, and its dysfunctions may be implicated in a variety of disease states associated with oxidative stress, including cancer and aging-associated pathologies. But, the precise mechanism is still obscure in various aspects of aging containing ovarian aging. Identification and relative quantification of the increased proteins affected by Prdx II deficiency may help identify novel signaling mechanisms that are important for oxidative stress-related diseases. To identify the increased proteins in Prdx $II^{-/-}$ mice, we performed RBC comparative proteome analysis in membrane fraction and cytosolic fractions by nano-UPLC-$MS^E$ shotgun proteomics. We found the increased 86 proteins in membrane (32 proteins) and cytosolic (54 proteins) fractions, and analyzed comparative expression pattern in healthy RBCs of Prdx $II^{+/+}$ mice, healthy RBCs of Prdx $II^{-/-}$ mice, and abnormal RBCs of Prdx $II^{-/-}$ mice. These proteins belonged to cellular functions related with RBC lifespan maintain, such as cellular morphology and assembly, cell-cell interaction, metabolism, and stress-induced signaling. Moreover, protein networks among the increased proteins were analyzed to associate with various diseases. Taken together, RBC proteome may provide clues to understand the clue about redox-imbalanced diseases.

• 농업과학연구
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• 제39권4호
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• pp.467-471
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• 2012

In this study, we investigated the antioxidative and antiaging activity of Perilla frutescens using LLC-$PK_1$ porcine renal epithelial cell and WI-38 human diploid fibroblast cell. The extract from Perilla frutescens showed strong protective effect against nitric oxide (NO) and superoxide ($O_2{^-}$)-induced oxidative stress generated by sodium nitroprusside (SNP) and pyrogallol, respectively. The result showed that P. frutescens increased the cell viability and showed scavenging activity of NO and $O_2{^-}$. In addition, the extract of P. frutescens exerted the protective effect against peroxynitrite ($ONOO^-$) induced by 3-morpholinosydnonimine. It suggests that P. frutescens would have the protective role against $ONOO^-$ itself and its precursors, NO and $O_2{^-}$. Furthermore, the aging model of hydrogen peroxide ($H_2O_2$)-treated WI-38 human diploid fibroblast was employed to investigate the anti-aging effect of P. frutescens. $H_2O_2$-treated WI-38 cells showed the loss of cell viability, however before-treatment with P. frutescens to WI-38 cells under premature senescence could delay the cellular aging process. The present study suggests the antioxidative and antiaging potential against free radical-induced oxidative damage of P. frutescens.

• Genomics & Informatics
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• 제3권2호
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• pp.66-72
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• 2005

The epidermis is a physiological barrier to protect organisms against environment. During the aging process, skin tissues undergo various changes including morphological and functional changes. The transcriptional regulation of genes is part of cellular reaction of aging process. In order to examine the changes of gene expression during the aging process, we used the primary cell culture system of human keratinocytes. Since UV radiation is the most important environmental skin aggressor, causing skin cancer and other problems including premature skin aging, we examined the changes of gene expression in human keratinocytes after UV irradiation using oligonucleotide microarray containing over 10,000 genes. We also compared the gene expression patterns of the senescent and UV treated cells. Expression of the variety of genes related to transcription factors, cell cycle regulation, immune response was altered in human keratinocytes. Some of down-regulated genes are represented in both senescent and UV treated cells. The results may provide a new view of gene expression following UVB exposure and aging process in human keratinocytes.

• 대한후두음성언어의학회지
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• 제25권1호
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• pp.20-23
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• 2014

Age-related changes in larynx can have a direct impact on voice quality and general comfort level. Observations of vocal aging have spanned perceptual, acoustic, aerodynamic, physical, electromyographic (EMG) and histological levels. Evidence of differential vocal aging in relation to gender and physical condition has been reported. Perceptual, acoustic, aerodynamic, kinematic, EMG and histological data document age-related changes in laryngeal structure and function with advancing age. These changes contribute to a functional age-related impact of vocal hypofunction or compensatory hyperfunction. This review will focus on the current understanding of the clinical and cellular changes in the larynx that lead to presbyphonia.