1.Telomerase Activity and Expression of MIB-1 and bcl-2 in Human Chorionic Villi from Early and Term Normal Pregnancy.
Jung Sook CHO ; Young Soon KANG ; In Gul MOON ; Bum Chae CHOI ; Jong Pyo LEE ; Hoon Taek LEE ; Sung Ran HONG
Korean Journal of Pathology 2000;34(11):927-933
Telomerase is an enzyme that maintains telomeres and prevents telomere shortening, and may be linked with cellular proliferation or the aging process. The purpose was to examine telomerase activity in human chorionic villi from early and term normal pregnancies, and to analyze the correlation of telomerase activity (TA) with MIB-1 & bcl-2. A total of 37 placentae were obtained from 16 early and 21 term pregnancies. TA was assayed by telomeric repeat amplification protocol, and immunohistochemical staining was performed for MIB-1 & bcl-2 expression. TA & MIB-1 expression were strong in early placenta, but bcl-2 was highly expressed in term placentae. Thirteen (81.25%) of 16 early placentae showed TA, but only 2 (9.52%) of 21 term placentae expressed TA (p<0.01). MIB-1 was observed in nuclei of cytotrophoblast, and the expression rate was 16.09% in early placentae and 2.87% in term placentae (p<0.01). bcl-2 was observed only in the cytoplasm of syncytiotrophoblast. Term placenta demonstrated stronger expression of bcl-2 compared to early placentae (p<0.05). These findings suggest that TA, MIB-1 & bcl-2 expression are critically regulated over the course of gestation: cytotrophoblast, main cells of early chorionic villi, may be a common source of telomerase and proliferative activity. The TA showed good correlation with cellular proliferative activity. Syncytiotrophoblast, may be a main source of bcl-2 expression which is stronger in the term placentae.
Aging
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Cell Proliferation
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Chorion*
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Chorionic Villi*
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Cytoplasm
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Humans*
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Placenta
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Pregnancy*
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Telomerase*
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Telomere
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Telomere Shortening
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Trophoblasts
2.Autophagy, Cellular Aging and Age-related Human Diseases
So Yeong CHEON ; Hyunjeong KIM ; David C RUBINSZTEIN ; Jong Eun LEE
Experimental Neurobiology 2019;28(6):643-657
Macroautophagy/autophagy is a conserved degradation system that engulfs intracytoplasmic contents, including aggregated proteins and organelles, which is crucial for cellular homeostasis. During aging, cellular factors suggested as the cause of aging have been reported to be associated with progressively compromised autophagy. Dysfunctional autophagy may contribute to age-related diseases, such as neurodegenerative disease, cancer, and metabolic syndrome, in the elderly. Therefore, restoration of impaired autophagy to normal may help to prevent age-related disease and extend lifespan and longevity. Therefore, this review aims to provide an overview of the mechanisms of autophagy underlying cellular aging and the consequent disease. Understanding the mechanisms of autophagy may provide potential information to aid therapeutic interventions in age-related diseases.
Aged
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Aging
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Autophagy
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Cell Aging
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DNA Damage
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Homeostasis
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Humans
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Longevity
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Neurodegenerative Diseases
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Organelles
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Oxidative Stress
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Telomere Shortening
3.Comparison of Hemoglobin Correction Effects According to Storage Period and Other Factors in the Transfusion of Packed Red Blood Cells in Neonatal Intensive Care Unit Patients.
Ji Hyun PARK ; Seom Gim KONG ; Yoo Rha HONG
Neonatal Medicine 2018;25(4):170-177
PURPOSE: Preterm infants frequently require red blood cell (RBC) transfusions in neonatal intensive care units (NICU). Storage RBCs undergo many changes during storage periods. We aimed to compare the hemoglobin (Hb) correction effect according to the period of RBC storage and investigate the factors influencing Hb correction. METHODS: This retrospective study reviewed the medical records of 289 patients who received RBC transfusion more than once in the NICU of Kosin University Gospel Hospital between February 2006 and March 2016. The subjects were classified into two storage groups: short-term (≤7 days, n=88) and long-term (>7 days, n=201), according to the period of RBC storage. We checked Hb levels by complete blood cell count tests conducted within 2 days before and 5 to 9 days after the first transfusion. We compared the Hb difference between the two groups and analyzed the factors influencing Hb correction. RESULTS: Excluding the use of an invasive ventilator, there was no significant difference between the two groups in terms of clinical characteristics. There was no significant difference in the Hb correction effect between the two groups (P=0.537). Birth weight greater than 1,500 g, higher weight at transfusion, and larger volume of transfusion were significant prognostic factors affecting greater changes in Hb. In addition, surgery experience, higher Hb level at transfusion, and additional blood tests were found to be significantly associated with less changes in Hb. CONCLUSION: The RBC storage period did not affect the Hb correction effect. The Hb correction effect may be diminished in infants with lower birth weight and lower weight at transfusion under unstable clinical conditions.
Birth Weight
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Blood Cell Count
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Erythrocyte Aging
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Erythrocyte Transfusion
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Erythrocytes*
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Hematologic Tests
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Humans
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Infant
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Infant, Newborn
;
Infant, Premature
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Intensive Care Units, Neonatal
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Intensive Care, Neonatal*
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Medical Records
;
Premature Birth
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Retrospective Studies
;
Ventilators, Mechanical
4.Telomere Biology in Mood Disorders: An Updated, Comprehensive Review of the Literature
Ather MUNEER ; Fareed Aslam MINHAS
Clinical Psychopharmacology and Neuroscience 2019;17(3):343-363
Major psychiatric disorders are linked to early mortality and patients afflicted with these ailments demonstrate an increased risk of developing physical diseases that are characteristically seen in the elderly. Psychiatric conditions like major depressive disorder, bipolar disorder and schizophrenia may be associated with accelerated cellular aging, indicated by shortened leukocyte telomere length (LTL), which could underlie this connection. Telomere shortening occurs with repeated cell division and is reflective of a cell’s mitotic history. It is also influenced by cumulative exposure to inflammation and oxidative stress as well as the availability of telomerase, the telomere-lengthening enzyme. Precariously short telomeres can cause cells to undergo senescence, apoptosis or genomic instability; shorter LTL correlates with compromised general health and foretells mortality. Important data specify that LTL may be reduced in principal psychiatric illnesses, possibly in proportion to exposure to the ailment. Telomerase, as measured in peripheral blood monocytes, has been less well characterized in psychiatric illnesses, but a role in mood disorder has been suggested by preclinical and clinical studies. In this manuscript, the most recent studies on LTL and telomerase activity in mood disorders are comprehensively reviewed, potential mediators are discussed, and future directions are suggested. An enhanced comprehension of cellular aging in psychiatric illnesses could lead to their re-conceptualizing as systemic ailments with manifestations both inside and outside the brain. At the same time this paradigm shift could identify new treatment targets, helpful in bringing about lasting cures to innumerable sufferers across the globe.
Aged
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Aging
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Apoptosis
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Biology
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Bipolar Disorder
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Brain
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Cell Aging
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Cell Division
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Comprehension
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Depressive Disorder, Major
;
Genomic Instability
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Humans
;
Inflammation
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Leukocytes
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Monocytes
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Mood Disorders
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Mortality
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Oxidative Stress
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Schizophrenia
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Telomerase
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Telomere Shortening
;
Telomere
5.Can we rejuvenate? Implications of biological aging research.
Yeungnam University Journal of Medicine 2017;34(1):1-10
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.
Aging*
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Cell Aging
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Humans
;
Population Characteristics
;
Rejuvenation
6.Can we rejuvenate? Implications of biological aging research
Yeungnam University Journal of Medicine 2017;34(1):1-10
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.
Aging
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Cell Aging
;
Humans
;
Population Characteristics
;
Rejuvenation
7.Kidneys with bad ends.
Journal of the Korean Society of Pediatric Nephrology 2008;12(1):11-22
Telomeres consist of tandem guanine-thymine(G-T) repeats in most eukaryotic chromosomes. Human telomeres are predominantly linear, double stranded DNA as they ended in 30-200 nucleotides(bases,b) 3'-overhangs. In DNA replication, removal of the terminal RNA primer from the lagging strand results in a 3'-overhang of uncopied DNA. This is because of bidirectional DNA replication and specificity of unidirectional DNA polymerase. After the replication, parental and daughter DNA strands have unequal lengths due to a combination of the end- replication problem and end-processing events. The gradual chromosome shortening is observed in most somatic cells and eventually leads to cellular senescence. Telomere shortening could be a molecular clock that signals the replicative senescence. The shortening of telomeric ends of human chromosomes, leading to sudden growth arrest, triggers DNA instability as biological switches. In addition, telomere dysfunction may cause chronic allograft nephropathy or kidney cancers. The renal cell carcinoma(RCC) in women may be less aggressive and have less genomic instability than in man. Younger patients with telomere dysfunction are at a higher risk for RCC than older patients. Thus, telomeres maintain the integrity of the genome and are involved in cellular aging and cancer. By studying the telomeric DNA, we may characterize the genetic determinants in diseases and discover the tools in molecular medicine.
Aging
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Cell Aging
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Chromosomes, Human
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DNA
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DNA Replication
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Female
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Genome
;
Genomic Instability
;
Humans
;
Kidney
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Kidney Neoplasms
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Molecular Medicine
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Nuclear Family
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Parents
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RNA
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Sensitivity and Specificity
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Telomere
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Telomere Shortening
;
Transplantation, Homologous
8.Aquatide Activation of SIRT1 Reduces Cellular Senescence through a SIRT1-FOXO1-Autophagy Axis.
Chae Jin LIM ; Yong Moon LEE ; Seung Goo KANG ; Hyung W LIM ; Kyong Oh SHIN ; Se Kyoo JEONG ; Yang Hoon HUH ; Suin CHOI ; Myungho KOR ; Ho Seong SEO ; Byeong Deog PARK ; Keedon PARK ; Jeong Keun AHN ; Yoshikazu UCHIDA ; Kyungho PARK
Biomolecules & Therapeutics 2017;25(5):511-518
Ultraviolet (UV) irradiation is a relevant environment factor to induce cellular senescence and photoaging. Both autophagy- and silent information regulator T1 (SIRT1)-dependent pathways are critical cellular processes of not only maintaining normal cellular functions, but also protecting cellular senescence in skin exposed to UV irradiation. In the present studies, we investigated whether modulation of autophagy induction using a novel synthetic SIRT1 activator, heptasodium hexacarboxymethyl dipeptide-12 (named as Aquatide), suppresses the UVB irradiation-induced skin aging. Treatment with Aquatide directly activates SIRT1 and stimulates autophagy induction in cultured human dermal fibroblasts. Next, we found that Aquatide-mediated activation of SIRT1 increases autophagy induction via deacetylation of forkhead box class O (FOXO) 1. Finally, UVB irradiation-induced cellular senescence measured by SA-β-gal staining was significantly decreased in cells treated with Aquatide in parallel to occurring SIRT1 activation-dependent autophagy. Together, Aquatide modulates autophagy through SIRT1 activation, contributing to suppression of skin aging caused by UV irradiation.
Autophagy
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Cell Aging*
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Fibroblasts
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Humans
;
Skin
;
Skin Aging
9.Profiling of genes in healthy hGF, aging hGF, healthy hPDLF and inflammatory hPDLF by DNA microarray.
Sang Jun YUN ; Byung Ock KIM ; Jeong Hun YUN ; Dong Wan KANG ; Hyun Seon JANG
The Journal of the Korean Academy of Periodontology 2006;36(3):767-782
No abstract available.
Aging*
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Cell Aging
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DNA*
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Oligonucleotide Array Sequence Analysis*
10.Immortalization of Primary Keratinocytes and Its Application to Skin Research.
Biomolecules & Therapeutics 2015;23(5):391-399
As a major component of the epidermal tissue, a primary keratinocyte has served as an essential tool not only for the study of pathogenesis of skin-related diseases but also for the assessment of potential toxicities of various chemicals used in cosmetics. However, its short lifespan in ex vivo setting has been a great hurdle for many practical applications. Therefore, a number of immortalization attempts have been made with success to overcome this limitation. In order to understand the immortalization process of a primary keratinocyte, several key biological phenomena governing its lifespan will be reviewed first. Then, various immortalization methods for the establishment of stable keratinocyte cell lines will be explained. Finally, its application to a three-dimensional skin culture system will be described.
Aging
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Biological Phenomena
;
Cell Line
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Keratinocytes*
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Skin*