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Journal articles on the topic 'Hayflick's limit'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Chen, Jun, and Michael S. Goligorsky. "Premature senescence of endothelial cells: Methusaleh's dilemma." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 5 (2006): H1729—H1739. http://dx.doi.org/10.1152/ajpheart.01103.2005.

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Senescence has been considered a programmed cellular response, parallel to apoptosis, that is turned on when a cell reaches Hayflick's limit. Once cells enter the senescence program, they cease to proliferate and undergo a series of morphological and functional changes. Studies support a central role for Rb protein in controlling this process after it receives senescent signals from the p53 and p16 pathways. Cellular senescence is considered an essential contributor to the aging process and has been shown to be an important tumor suppression mechanism. In addition, emerging evidence suggests t

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2

Gillooly, James F., April Hayward, Chen Hou, and J. Gordon Burleigh. "Explaining differences in the lifespan and replicative capacity of cells: a general model and comparative analysis of vertebrates." Proceedings of the Royal Society B: Biological Sciences 279, no. 1744 (2012): 3976–80. http://dx.doi.org/10.1098/rspb.2012.1129.

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A better understanding of the factors that govern individual cell lifespan and the replicative capacity of cells (i.e. Hayflick's limit) is important for addressing disease progression and ageing. Estimates of cell lifespan in vivo and the replicative capacity of cell lines in culture vary substantially both within and across species, but the underlying reasons for this variability remain unclear. Here, we address this issue by presenting a quantitative model of cell lifespan and cell replicative capacity. The model is based on the relationship between cell mortality and metabolic rate, which

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3

Franken, Jessica. "The Hayflick Limit." River Teeth: A Journal of Nonfiction Narrative 22, no. 2 (2021): 107–11. http://dx.doi.org/10.1353/rvt.2021.0010.

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4

Luft, Friedrich C. "Approaching the Hayflick limit." Trends in Cardiovascular Medicine 25, no. 3 (2015): 240–42. http://dx.doi.org/10.1016/j.tcm.2014.12.008.

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5

Shay, Jerry W., and Woodring E. Wright. "Hayflick, his limit, and cellular ageing." Nature Reviews Molecular Cell Biology 1, no. 1 (2000): 72–76. http://dx.doi.org/10.1038/35036093.

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6

Griffiths, Paul D. "Herpesviruses and the Hayflick Limit In Vivo." Journal of Infectious Diseases 216, no. 5 (2017): 511–13. http://dx.doi.org/10.1093/infdis/jix256.

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7

Gill, Zoe, Martin Nieuwoudt, and Wilfred Ndifon. "The Hayflick Limit and Age-Related Adaptive Immune Deficiency." Gerontology 64, no. 2 (2017): 135–39. http://dx.doi.org/10.1159/000478091.

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The adaptive immune system (AIS) acquires significant deficiency during chronological ageing, making older individuals more susceptible to infections and less responsive to vaccines compared to younger individuals. At the cellular level, one of the most striking features of this ageing-related immune deficiency is the dramatic loss of T-cell diversity that occurs in elderly humans. After the age of 70 years, there is a sharp decline in the diversity of naïve T cells, including a >10-fold decrease in the CD4+ compartment and a >100-fold decrease in the CD8+ compartment. Such changes are d

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8

Watts, Geoff. "Leonard Hayflick and the limits of ageing." Lancet 377, no. 9783 (2011): 2075. http://dx.doi.org/10.1016/s0140-6736(11)60908-2.

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9

Migliaccio, Giovanni, Massimo Sanchez, Francesca Masiello та ін. "the γ Isoform of the Glucocorticoid Receptor Is Ontogenetically Activated and Predicts Poor Ex-Vivo Expansion of Erythroid Cells From Adult Blood." Blood 114, № 22 (2009): 642. http://dx.doi.org/10.1182/blood.v114.22.642.642.

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Abstract Abstract 642 Ex-vivo generated erythroblasts (EBs) represent alternative transfusion products. Adult blood (AB) contains numbers of progenitor cells comparable to those present in cord blood (CB) (106 vs 1.8×106 CD34pos cells in average AB and CB donations) but generates lower numbers of erythroblasts (EBs) (∼4.8×108 vs 6.6×1010, respectively) and, in spite of its numerous advantages, is not considered suitable for ex-vivo EB production. To assess the potential of AB to generate EBs ex-vivo, the growth factors [stem cell factor (SCF), interleukin-3 (IL-3) and erythropoietin (EPO)] and

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10

Ndifon, Wilfred, and Jonathan Dushoff. "The Hayflick Limit May Determine the Effective Clonal Diversity of Naive T Cells." Journal of Immunology 196, no. 12 (2016): 4999–5004. http://dx.doi.org/10.4049/jimmunol.1502343.

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11

Effros, Rita B., and Graham Pawelec. "Replicative senescence of T cells: does the Hayflick Limit lead to immune exhaustion?" Immunology Today 18, no. 9 (1997): 450–54. http://dx.doi.org/10.1016/s0167-5699(97)01079-7.

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12

Pilyugin, Sergei, John Mittler, and Rustom Antia. "Modeling T-cell Proliferation: an Investigation of the Consequences of the Hayflick Limit." Journal of Theoretical Biology 186, no. 1 (1997): 117–29. http://dx.doi.org/10.1006/jtbi.1996.0319.

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13

Suchánek, Jakub, Tomáš Soukup, Romana Ivančaková, et al. "Human Dental Pulp Stem Cells – Isolation and Long Term Cultivation." Acta Medica (Hradec Kralove, Czech Republic) 50, no. 3 (2007): 195–201. http://dx.doi.org/10.14712/18059694.2017.82.

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Human adult mesenchymal stem cells (MSCs) are rare elements living in various organs (e.g. bone marrow, skeletal muscle), with capability to differentiate in various cell types (e.g. chondrocytes, adipocytes and osteoblasts). In the year 2000, Gronthos and co-workers isolated stem cells from the human dental pulp (DPSCs). Later on, stem cells from exfoliated tooth were also obtained. The aims of our study were to establish protocol of DPSCs isolation and to cultivate DPSCs either from adult or exfoliated tooth, and to compare these cells with mesenchymal progenitor cell (MPCs) cultures. MPCs w

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14

Juckett, David A. "Cellular aging (The hayflick limit) and species longevity: A unification model based on clonal succession." Mechanisms of Ageing and Development 38, no. 1 (1987): 49–71. http://dx.doi.org/10.1016/0047-6374(87)90110-2.

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15

Effros, Rita B. "Impact of the Hayflick Limit on T cell responses to infection: lessons from aging and HIV disease." Mechanisms of Ageing and Development 125, no. 2 (2004): 103–6. http://dx.doi.org/10.1016/j.mad.2003.11.003.

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16

Macieira-Coelho, A. "The Implications of the ‘Hayflick Limit’ for Aging of the Organism Have Been Misunderstood by Many Gerontologists." Gerontology 41, no. 2 (1995): 94–97. http://dx.doi.org/10.1159/000213669.

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17

Trubitsyn, A. G. "The mechanism of phenoptosis: 2. The Hayflick limit is caused by programmed decrease of the bioenergetics level." Advances in Gerontology 1, no. 2 (2011): 134–39. http://dx.doi.org/10.1134/s2079057011020147.

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18

Soukup, Tomáš, Jaroslav Mokrý, Jana Karbanová, Robert Pytlík, Petr Suchomel, and Lenka Kučerová. "Mesenchymal Stem Cells Isolated from the Human Bone Marrow: Cultivation, Phenotypic Analysis and Changes in Proliferation Kinetics." Acta Medica (Hradec Kralove, Czech Republic) 49, no. 1 (2006): 27–33. http://dx.doi.org/10.14712/18059694.2017.106.

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Mesenchymal Stem Cells (MSCs) are rare elements living in various organs (e.g., bone marrow), able to differentiate into specialized tissues, such as bone, cartilage, tendon, and myocardium. Since the first description of MSCs by Fridenshtein, several investigators have shown that these cells can also differentiate into chondrocytes, adipocytes, and, at least, in rodents into skeletal myoblasts. Later on, more primitive progenitor cells were characterized, able to give rise not only to limb-bud mesoderm, but also to cells of visceral mesoderm. Those cells were named mesodermal progenitor cells

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19

Effros, Rita B. "Replicative Senescence in the Immune System: Impact of the Hayflick Limit on T-Cell Function in the Elderly." American Journal of Human Genetics 62, no. 5 (1998): 1003–7. http://dx.doi.org/10.1086/301845.

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20

Golubev, A., S. Khrustalev, and A. Butov. "An in silico investigation into the causes of telomere length heterogeneity and its implications for the Hayflick limit." Journal of Theoretical Biology 225, no. 2 (2003): 153–70. http://dx.doi.org/10.1016/s0022-5193(03)00229-7.

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21

Liu, Jun, Lihui Wang, Zhiguo Wang, and Jun-Ping Liu. "Roles of Telomere Biology in Cell Senescence, Replicative and Chronological Ageing." Cells 8, no. 1 (2019): 54. http://dx.doi.org/10.3390/cells8010054.

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Telomeres with G-rich repetitive DNA and particular proteins as special heterochromatin structures at the termini of eukaryotic chromosomes are tightly maintained to safeguard genetic integrity and functionality. Telomerase as a specialized reverse transcriptase uses its intrinsic RNA template to lengthen telomeric G-rich strand in yeast and human cells. Cells sense telomere length shortening and respond with cell cycle arrest at a certain size of telomeres referring to the “Hayflick limit.” In addition to regulating the cell replicative senescence, telomere biology plays a fundamental role in

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22

Jim, Carol, and Simon Berkovich. "Labeling of Chromosomes in Cell Development and the Appearance of Monozygotic Twins." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/628092.

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Understanding the mechanism behind the structure of the internal cellular clock can lead to advances in the knowledge of origins of pairs of monozygotic twins and higher order multiples as well as other biological phenomena. To gain insight into this mechanism, we analyze possible cell labeling schemes that model an organism’s development. Our findings lead us to predict that monozygotic quadruplets are not quadruplets in the traditional sense but rather two pairs of monozygotic twins where the pairs slightly differ—a situation we coin quadruplet twins. From the considered model, the probabili

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23

RASNICK, David. "Auto-catalysed progression of aneuploidy explains the Hayflick limit of cultured cells, carcinogen-induced tumours in mice, and the age distribution of human cancer." Biochemical Journal 348, no. 3 (2000): 497. http://dx.doi.org/10.1042/0264-6021:3480497.

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24

RASNICK, David. "Auto-catalysed progression of aneuploidy explains the Hayflick limit of cultured cells, carcinogen-induced tumours in mice, and the age distribution of human cancer." Biochemical Journal 348, no. 3 (2000): 497–506. http://dx.doi.org/10.1042/bj3480497.

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Evidence continues to accumulate that aneuploidy, an imbalance in the number of chromosomes, is responsible for the characteristic phenotypes of cancer, including the abnormal cellular size and morphology of cancer cells, the appearance of tumour-associated antigens, as well as the high levels of membrane-bound and secreted proteins responsible for invasiveness and loss of contact inhibition. Aneuploidy has also been demonstrated to be the self-perpetuating source of the karyotypic instability of cancer cells. Here it is shown that the auto-catalysed progression of aneuploidy explains the kine

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25

Rubtsova, M. P., D. P. Vasilkova, A. N. Malyavko, Yu V. Naraikina, M. I. Zvereva, and O. A. Dontsova. "Telomere Lengthening and Other Functions of Telomerase." Acta Naturae 4, no. 2 (2012): 44–61. http://dx.doi.org/10.32607/20758251-2012-4-2-44-61.

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Telomerase is an enzyme that maintains the length of the telomere. The telomere length specifies the number of divisions a cell can undergo before it finally dies (i.e. the proliferative potential of cells). For example, telomerase is activated in embryonic cell lines and the telomere length is maintained at a constant level; therefore, these cells have an unlimited fission potential. Stem cells are characterized by a lower telomerase activity, which enables only partial compensation for the shortening of telomeres. Somatic cells are usually characterized by the absence of telomerase activity.

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26

Rubtsova, M. P., D. P. Vasilkova, A. N. Malyavko, Yu V. Naraikina, M. I. Zvereva, and O. A. Dontsova. "Telomere Lengthening and Other Functions of Telomerase." Acta Naturae 4, no. 2 (2012): 44–61. http://dx.doi.org/10.32607/actanaturae.10630.

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Telomerase is an enzyme that maintains the length of the telomere. The telomere length specifies the number of divisions a cell can undergo before it finally dies (i.e. the proliferative potential of cells). For example, telomerase is activated in embryonic cell lines and the telomere length is maintained at a constant level; therefore, these cells have an unlimited fission potential. Stem cells are characterized by a lower telomerase activity, which enables only partial compensation for the shortening of telomeres. Somatic cells are usually characterized by the absence of telomerase activity.

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27

Naveilhan, P., C. Baudet, W. Jabbour, and D. Wion. "A theory that may explain the Hayflick limit — a means to delete one copy of a repeating sequence during each cell cycle in certain human cells such as fibroblasts." Mechanisms of Ageing and Development 75, no. 3 (1994): 205–13. http://dx.doi.org/10.1016/0047-6374(94)90010-8.

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28

Zijlmans, Mark, Susan Swiggers, Maria Rife Soler, and Berna Beverloo. "Replicative Senescence in Good-Risk Acute Myeloid Leukemia." Blood 108, no. 11 (2006): 1922. http://dx.doi.org/10.1182/blood.v108.11.1922.1922.

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Abstract Immortal cell growth is considered the hallmark of tumor cells. In contrast, normal cells have a limited proliferative capacity of 40–60 cell divisions, also known as the Hayflick limit. The limited proliferative capacity of normal cells relates to gradual telomere shortening as a consequence of the end-replication problem. Upon critical telomere shortening, cells enter a non-replicative but viable state referred to as replicative senescence. These replicative senescent cells stain blue in a beta-Galactosidase assay and activate DNA double-strand break repair pathways at telomeres (e.

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29

Nilsson, Ola, Robert D. Mitchum, Lenneke Schrier, et al. "Growth plate senescence is associated with loss of DNA methylation." Journal of Endocrinology 186, no. 1 (2005): 241–49. http://dx.doi.org/10.1677/joe.1.06016.

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The overall body size of vertebrates is primarily determined by longitudinal bone growth at the growth plate. With age, the growth plate undergoes programmed senescence, causing longitudinal bone growth to slow and eventually cease. Indirect evidence suggests that growth plate senescence occurs because stem-like cells in the growth plate resting zone have a finite proliferative capacity that is gradually exhausted. Similar limits on replication have been observed when many types of animal cells are placed in cell culture, an effect known as the Hayflick phenomenon. However, we found that the n

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30

Wang, Lulu, Zheng Liu, Dongni Huang та ін. "IL-37 Exerts Anti-Inflammatory Effects in Fetal Membranes of Spontaneous Preterm Birth via the NF-κB and IL-6/STAT3 Signaling Pathway". Mediators of Inflammation 2020 (11 липня 2020): 1–15. http://dx.doi.org/10.1155/2020/1069563.

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Spontaneous preterm birth (sPTB), defined as delivery before 37 weeks of gestation, is thought to be a multifactorial syndrome. However, the inflammatory imbalance at the maternal-fetal interface promotes excessive secretion of inflammatory factors and induces apoptosis and degradation of the extracellular matrix (ECM), which can subsequently lead to preterm birth. As an anti-inflammatory molecule in the IL-1 family, interleukin-37 (IL-37) mainly plays an inhibiting role in a variety of inflammatory diseases. However, as a typical inflammatory disease, no previous studies have been carried out

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31

Shveid Gerson, Daniela, Alejandro Zentella - Dehesa, Raquel Gerson Cwilich, et al. "Creation of a primary breast cancer culture repository from patients with a BMI >30 kg/m2: A Mexican endeavor." Journal of Clinical Oncology 39, no. 15_suppl (2021): e12574-e12574. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e12574.

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e12574 Background: Currently there are no primary cultures or cell lines derived from patients with breast cancer and obesity. It has been postulated that breast cancer in obese women behaves differently as it does in non-obese women, as is composed of distinct biological features, as was generated in a different metabolic environment, as well as pertains to a different prognosis and different response to chemotherapy, lower rates of overall survival and a greater probability of recurrence. By creating a primary breast cancer culture bank of breast cancer tumors from women with obesity (BMI &g

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32

Skopec, Robert. "Cancer, Hayflick limit and the Entscheidungsproblem." Global Vaccines and Immunology 2, no. 2 (2017). http://dx.doi.org/10.15761/gvi.1000127.

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33

Schmutz, Isabelle, Arjen R. Mensenkamp, Kaori K. Takai, et al. "TINF2 is a haploinsufficient tumor suppressor that limits telomere length." eLife 9 (December 1, 2020). http://dx.doi.org/10.7554/elife.61235.

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Telomere shortening is a presumed tumor suppressor pathway that imposes a proliferative barrier (the Hayflick limit) during tumorigenesis. This model predicts that excessively long somatic telomeres predispose to cancer. Here, we describe cancer-prone families with two unique TINF2 mutations that truncate TIN2, a shelterin subunit that controls telomere length. Patient lymphocyte telomeres were unusually long. We show that the truncated TIN2 proteins do not localize to telomeres, suggesting that the mutations create loss-of-function alleles. Heterozygous knock-in of the mutations or deletion o

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34

Lee, Kyung Hyun, and Marek Kimmel. "Analysis of two mechanisms of telomere maintenance based on the theory of g-Networks and stochastic automata networks." BMC Genomics 21, S9 (2020). http://dx.doi.org/10.1186/s12864-020-06937-9.

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Abstract * Background Telomeres, which are composed of repetitive nucleotide sequences at the end of chromosomes, behave as a division clock that measures replicative senescence. Under the normal physiological condition, telomeres shorten with each cell division, and cells use the telomere lengths to sense the number of divisions. Replicative senescence has been shown to occur at approximately 50–70 cell divisions, which is termed the Hayflick’s limit. However, in cancer cells telomere lengths are stabilized, thereby allowing continual cell replication by two known mechanisms: activation of te

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