Academic literature on the topic 'Senescence markers'

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Journal articles on the topic "Senescence markers"

1

Adewoye, Adeolu Badi, Dimitris Tampakis, Antonia Follenzi, and Alexandra Stolzing. "Multiparameter flow cytometric detection and quantification of senescent cells in vitro." Biogerontology 21, no. 6 (2020): 773–86. http://dx.doi.org/10.1007/s10522-020-09893-9.

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Abstract It has been over half a century since cellular senescence was first noted and characterized, and yet no consensus senescent marker has been reliably established. This challenge is compounded by the complexity and heterogenic phenotypes of senescent cells. This necessitates the use of multiple biomarkers to confidently characterise senescent cells. Despite cytochemical staining of senescence associated-beta-galactosidase being a single marker approach, as well as being time and labour-intensive, it remains the most popular detection method. We have developed an alternative flow cytomet
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2

Bojko, Agnieszka, Joanna Czarnecka-Herok, Agata Charzynska, Michal Dabrowski, and Ewa Sikora. "Diversity of the Senescence Phenotype of Cancer Cells Treated with Chemotherapeutic Agents." Cells 8, no. 12 (2019): 1501. http://dx.doi.org/10.3390/cells8121501.

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It is acknowledged that cancer cells are able to undergo senescence in response to clinically used chemotherapeutics. Moreover, recent years have provided evidence that some drugs can selectively remove senescent cells. Therefore, it is essential to properly identify and characterize senescent cells, especially when it comes to cancer. Senescence was induced in various cancer cell lines (A549, SH-SY-5Y, HCT116, MDA-MB-231, and MCF-7) following treatment with doxorubicin, irinotecan, methotrexate, 5-fluorouracil, oxaliplatin, or paclitaxel. Treatment with tested chemotherapeutics resulted in up
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3

Verma, Dinesh Kumar, Bo Am Seo, Anurupa Ghosh, et al. "Alpha-Synuclein Preformed Fibrils Induce Cellular Senescence in Parkinson’s Disease Models." Cells 10, no. 7 (2021): 1694. http://dx.doi.org/10.3390/cells10071694.

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Emerging evidence indicates that cellular senescence could be a critical inducing factor for aging-associated neurodegenerative disorders. However, the involvement of cellular senescence remains unclear in Parkinson’s disease (PD). To determine this, we assessed the effects of α-synuclein preformed fibrils (α-syn PFF) or 1-methyl-4-phenylpyridinium (MPP+) on changes in cellular senescence markers, employing α-syn PFF treated-dopaminergic N27 cells, primary cortical neurons, astrocytes and microglia and α-syn PFF-injected mouse brain tissues, as well as human PD patient brains. Our results demo
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4

Kim, Seo Rin, Kai Jiang, Christopher M. Ferguson, et al. "Transplanted senescent renal scattered tubular-like cells induce injury in the mouse kidney." American Journal of Physiology-Renal Physiology 318, no. 5 (2020): F1167—F1176. http://dx.doi.org/10.1152/ajprenal.00535.2019.

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Cellular senescence, a permanent arrest of cell proliferation, is characterized by a senescence-associated secretory phenotype (SASP), which reinforces senescence and exerts noxious effects on adjacent cells. Recent studies have suggested that transplanting small numbers of senescent cells suffices to provoke tissue inflammation. We hypothesized that senescent cells can directly augment renal injury. Primary scattered tubular-like cells (STCs) acquired from pig kidneys were irradiated by 10 Gy of cesium radiation, and 3 wk later cells were characterized for levels of senescence and SASP marker
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5

Kritsilis, Marios, Sophia V. Rizou, Paraskevi Koutsoudaki, Konstantinos Evangelou, Vassilis Gorgoulis, and Dimitrios Papadopoulos. "Ageing, Cellular Senescence and Neurodegenerative Disease." International Journal of Molecular Sciences 19, no. 10 (2018): 2937. http://dx.doi.org/10.3390/ijms19102937.

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Ageing is a major risk factor for developing many neurodegenerative diseases. Cellular senescence is a homeostatic biological process that has a key role in driving ageing. There is evidence that senescent cells accumulate in the nervous system with ageing and neurodegenerative disease and may predispose a person to the appearance of a neurodegenerative condition or may aggravate its course. Research into senescence has long been hindered by its variable and cell-type specific features and the lack of a universal marker to unequivocally detect senescent cells. Recent advances in senescence mar
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6

Coates, Philip J. "Markers of senescence?" Journal of Pathology 196, no. 4 (2002): 371–73. http://dx.doi.org/10.1002/path.1073.

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7

Wagner, Kay-Dietrich, and Nicole Wagner. "The Senescence Markers p16INK4A, p14ARF/p19ARF, and p21 in Organ Development and Homeostasis." Cells 11, no. 12 (2022): 1966. http://dx.doi.org/10.3390/cells11121966.

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It is widely accepted that senescent cells accumulate with aging. They are characterized by replicative arrest and the release of a myriad of factors commonly called the senescence-associated secretory phenotype. Despite the replicative cell cycle arrest, these cells are metabolically active and functional. The release of SASP factors is mostly thought to cause tissue dysfunction and to induce senescence in surrounding cells. As major markers for aging and senescence, p16INK4, p14ARF/p19ARF, and p21 are established. Importantly, senescence is also implicated in development, cancer, and tissue
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8

Kim, Gee-Hye, Yun Kyung Bae, Ji Hye Kwon, et al. "Positively Correlated CD47 Activation and Autophagy in Umbilical Cord Blood-Derived Mesenchymal Stem Cells during Senescence." Stem Cells International 2021 (April 15, 2021): 1–13. http://dx.doi.org/10.1155/2021/5582792.

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Autophagy plays a critical role in stem cell maintenance and is related to cell growth and cellular senescence. It is important to find a quality-control marker for predicting senescent cells. This study verified that CD47 could be a candidate to select efficient mesenchymal stem cells (MSCs) to enhance the therapeutic effects of stem cell therapy by analyzing the antibody surface array. CD47 expression was significantly decreased during the expansion of MSCs in vitro ( p < 0.01 ), with decreased CD47 expression correlated with accelerated senescence phenotype, which affected cell growth. U
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9

Rossi, Clara, Marco Venturin, Jakub Gubala, et al. "PURPL and NEAT1 Long Non-Coding RNAs Are Modulated in Vascular Smooth Muscle Cell Replicative Senescence." Biomedicines 11, no. 12 (2023): 3228. http://dx.doi.org/10.3390/biomedicines11123228.

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Cellular senescence is characterized by proliferation and migration exhaustion, senescence-associated secretory phenotype (SASP), and oxidative stress. Senescent vascular smooth muscle cells (VSMCs) contribute to cardiovascular diseases and atherosclerotic plaque instability. Since there are no unanimously agreed senescence markers in human VSMCs, to improve our knowledge, we looked for new possible senescence markers. To this end, we first established and characterized a model of replicative senescence (RS) in human aortic VSMCs. Old cells displayed several established senescence-associated m
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10

Galvis, Daniel, Darren Walsh, Lorna W. Harries, Eva Latorre, and James Rankin. "A dynamical systems model for the measurement of cellular senescence." Journal of The Royal Society Interface 16, no. 159 (2019): 20190311. http://dx.doi.org/10.1098/rsif.2019.0311.

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Senescent cells provide a good in vitro model to study ageing. However, cultures of ‘senescent’ cells consist of a mix of cell subtypes (proliferative, senescent, growth-arrested and apoptotic). Determining the proportion of senescent cells is crucial for studying ageing and developing new anti-degenerative therapies. Commonly used markers such as doubling population, senescence-associated β-galactosidase, Ki-67, γH2AX and TUNEL assays capture diverse and overlapping cellular populations and are not purely specific to senescence. A newly developed dynamical systems model follows the transition
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