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Journal articles on the topic 'Senescence markers'

Author: Grafiati

Published: 13 April 2024

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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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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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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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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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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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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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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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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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Frescas, David, Christelle M. Roux, Semra Aygun-Sunar, et al. "Senescent cells expose and secrete an oxidized form of membrane-bound vimentin as revealed by a natural polyreactive antibody." Proceedings of the National Academy of Sciences 114, no. 9 (2017): E1668—E1677. http://dx.doi.org/10.1073/pnas.1614661114.

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Studying the phenomenon of cellular senescence has been hindered by the lack of senescence-specific markers. As such, detection of proteins informally associated with senescence accompanies the use of senescence-associated β-galactosidase as a collection of semiselective markers to monitor the presence of senescent cells. To identify novel biomarkers of senescence, we immunized BALB/c mice with senescent mouse lung fibroblasts and screened for antibodies that recognized senescence-associated cell-surface antigens by FACS analysis and a newly developed cell-based ELISA. The majority of antibodi

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Chen, Jian, Jing Wang, Matt Lucas, et al. "Abstract B022: Targeting senescence cells in cancer and aging by conditionally active biologic therapeutics." Cancer Research 83, no. 2_Supplement_1 (2023): B022. http://dx.doi.org/10.1158/1538-7445.agca22-b022.

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Abstract Cellular senescence is characterized by stable cell cycle arrest and a secretory program that modulates the tissue microenvironment. The aberrant accumulation of senescent cells in aged and cancerous tissue triggers inflammatory signaling through a senescence-associated secretory phenotype (SASP), promoting aging and tumor progression. Pharmacologically, clearing senescent cells has been shown to have promising effects against cancer and age-related pathologies in preclinical models as well as human pilot clinical trials. However, current senescent cell elimination strategies are focu

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Bernadotte, Alexandra, Victor M. Mikhelson, and Irina M. Spivak. "Markers of cellular senescence. Telomere shortening as a marker of cellular senescence." Aging 8, no. 1 (2016): 3–11. http://dx.doi.org/10.18632/aging.100871.

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14

Yang, Niuxin, Masato Nakagawa, Aki Nishiura, et al. "Identification of Senescent Cells in Peri-Implantitis and Prevention of Mini-Implant Loss Using Senolytics." International Journal of Molecular Sciences 24, no. 3 (2023): 2507. http://dx.doi.org/10.3390/ijms24032507.

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Peri-implantitis is a disease that causes the detachment of orthodontic mini-implants. Recently, stress-induced senescent cells have been reported to be involved in various inflammatory diseases. Senescent cell-eliminating drugs, termed “senolytics”, can improve the symptoms of such diseases. However, the relationship between peri-implantitis and senescent cells remains unclear. In this study, we evaluated the presence of senescent cells in a rat peri-implantitis model developed with a gum ring. The effect on bone resorption and implant loss was also investigated with and without senolytics (D

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Kawka, Edyta, Janusz Witowski, Pilar Sandoval, et al. "Epithelial-To-Mesenchymal Transition and Migration of Human Peritoneal Mesothelial Cells Undergoing Senescence." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 39, no. 1 (2019): 35–41. http://dx.doi.org/10.3747/pdi.2017.00244.

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Background Epithelial-to-mesenchymal transition (EMT) of human peritoneal mesothelial cells (HPMCs) contributes to fibrotic thickening of the peritoneum that develops in patients on peritoneal dialysis (PD). The process is thought to be largely mediated by transforming growth factor-beta (TGF-β). As TGF-β has also been implicated in senescence of HPMCs, we have performed an exploratory study to examine if senescent HPMCs can undergo EMT. Methods Omentum-derived HPMCs were rendered senescent by repeated passages in culture. Features of EMT were assessed by immunostaining and quantitative polyme

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Norton, Emma J., Leslie R. Bridges, Lawrence C. Kenyon, Margaret M. Esiri, Dorothy C. Bennett, and Atticus H. Hainsworth. "Cell Senescence and Cerebral Small Vessel Disease in the Brains of People Aged 80 Years and Older." Journal of Neuropathology & Experimental Neurology 78, no. 11 (2019): 1066–72. http://dx.doi.org/10.1093/jnen/nlz088.

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Abstract Cerebral small vessel disease (cSVD) in penetrating arteries is a major cause of age-related morbidity. Cellular senescence is a molecular process targeted by novel senolytic drugs. We quantified senescence in penetrating arteries and tested whether myocyte senescence was associated with cSVD. We immunolabeled subcortical white matter of older persons (age 80–96 years, n = 60) with minimal AD, using antibodies to 2 established senescence markers (H3K9me3, γH2AX) and a myocyte marker (hSMM). Within the walls of penetrating arteries (20–300 µm), we quantified senescence-associated heter

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Choi, Eun-Jeong, In Sup Kil, and Eun-Gyung Cho. "Extracellular Vesicles Derived from Senescent Fibroblasts Attenuate the Dermal Effect on Keratinocyte Differentiation." International Journal of Molecular Sciences 21, no. 3 (2020): 1022. http://dx.doi.org/10.3390/ijms21031022.

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The skin is a multilayered and primary defensive organ. Intimate intercellular communication in the skin is necessary to ensure effective surveillance. Extracellular vesicles (EVs) are being explored for their involvement in intercellular skin communication. The aim of this study was to evaluate how human dermal fibroblasts (HDFs) accelerate EV production during senescence and the effects of senescence-associated EVs on epidermal homeostasis. Replicative senescent HDFs were assessed with senescence-associated β-galactosidase staining and the expression of senescence-related markers. Isolated E

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Dewald, Hannah K., Ricardo Iván Martínez-Zamudio, Themistoklis Vasilopoulos, Joycelyn Radeny, Utz Herbig та Patricia Fitzgerald-Bocarsly. "Senescence-associated β-galactosidase activity and other markers of senescence are present in human peripheral blood CD8+ cells during healthy aging". Journal of Immunology 206, № 1_Supplement (2021): 98.31. http://dx.doi.org/10.4049/jimmunol.206.supp.98.31.

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Abstract Aging is associated with a decline in the immune system, termed “immunosenescence”. Cellular senescence is defined by persistent cellular growth arrest and overall loss of function. If immune cells undergo cellular senescence in vivo, and if it has a role in immunosenesence, remains controversial due to the lack of specific markers to identify these cells. Human CD8+ T cells from younger and older donors were isolated from blood and labeled with a fluorescent substrate for senescence-associated b-galactosidase (SA-βGal). CD8+ T cells were sorted based on SA-βGal and analyzed by qRT-PC

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Dewald, Hannah K., Ricardo Iván Martínez-Zamudio, Themistoklis Vasilopoulos, Utz Herbig та Patricia Fitzgerald-Bocarsly. "Senescence-associated β-galactosidase activity and other markers of senescence are present in human peripheral blood mononuclear cells during healthy aging". Journal of Immunology 204, № 1_Supplement (2020): 154.15. http://dx.doi.org/10.4049/jimmunol.204.supp.154.15.

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Abstract Aging is associated with a decline in the immune system, termed “immunosenescence”. Cellular senescence is defined by persistent cellular growth arrest and overall loss of function. If immune cells undergo cellular senescence in vivo and whether cellular senescence has a role in immunosenesence remains controversial due to the lack of specific markers to reliably identify these cells in blood. Freshly isolated human peripheral blood mononuclear cells from younger and older donors were fluorescently labeled for senescence-associated β-galactosidase (SA-βGal). CD8+ T cells were sorted b

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Macieira-Coelho, A. "Markers of `cell senescence'." Mechanisms of Ageing and Development 103, no. 1 (1998): 105–9. http://dx.doi.org/10.1016/s0047-6374(98)00038-4.

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Martyshkina, Yuliya S., Valeriy P. Tereshchenko, Daria A. Bogdanova, and Stanislav A. Rybtsov. "Reliable Hallmarks and Biomarkers of Senescent Lymphocytes." International Journal of Molecular Sciences 24, no. 21 (2023): 15653. http://dx.doi.org/10.3390/ijms242115653.

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The phenomenon of accumulation of senescent adaptive immunity cells in the elderly is attracting attention due to the increasing risk of global epidemics and aging of the global population. Elderly people are predisposed to various infectious and age-related diseases and are at higher risk of vaccination failure. The accumulation of senescent cells increases age-related background inflammation, “Inflammaging”, causing lymphocyte exhaustion and cardiovascular, neurodegenerative, autoimmune and cancer diseases. Here, we present a comprehensive contemporary review of the mechanisms and phenotype

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Kaur, Gagandeep, Isaac K. Sundar, and Irfan Rahman. "p16-3MR: A Novel Model to Study Cellular Senescence in Cigarette Smoke-Induced Lung Injuries." International Journal of Molecular Sciences 22, no. 9 (2021): 4834. http://dx.doi.org/10.3390/ijms22094834.

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Cellular senescence and lung aging are associated with the pathogenesis of chronic obstructive pulmonary disease (COPD). COPD progresses with aging, and chronic smoking is the key susceptibility factor in lung pathological changes concurrent with mitochondrial dysfunction and biological aging. However, these processes involving cigarette smoke (CS)-mediated lung cellular senescence are difficult to distinguish. One of the impediments to studying cellular senescence in relation to age-related lung pathologies is the lack of a suitable in vivo model. In view of this, we provide evidence that sup

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Chen, Jian, Christina Wheeler, Jing Wang, et al. "Abstract 4795: Conditionally active biologics eliminates senescence cells in cancer and aging." Cancer Research 83, no. 7_Supplement (2023): 4795. http://dx.doi.org/10.1158/1538-7445.am2023-4795.

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Abstract The aberrant accumulation of senescent cells in aged and cancerous tissue triggers inflammatory signaling through a senescence-associated secretory phenotype (SASP), promoting aging and tumor progression. Pharmacologically, clearing senescent cells has been shown to have promising effects against cancer and age-related pathologies in preclinical models as well as early human clinical trials. However, current senescent cell elimination strategies are focused on targets that do not distinguish between hyper-inflamed or SASP senescent cells versus relatively non-inflamed senescent cells.

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Fischer, Bernard M., Jessica K. Wong, Simone Degan, et al. "Increased expression of senescence markers in cystic fibrosis airways." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 6 (2013): L394—L400. http://dx.doi.org/10.1152/ajplung.00091.2012.

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Cystic Fibrosis (CF) is a chronic lung disease characterized by chronic neutrophilic airway inflammation and increased levels of neutrophil elastase (NE) in the airways. We have previously reported that NE treatment triggers cell cycle arrest. Cell cycle arrest can lead to senescence, a complete loss of replicative capacity. Importantly, senescent cells can be proinflammatory and would perpetuate CF chronic inflammation. By immunohistochemistry, we evaluated whether airway sections from CF and control subjects expressed markers of senescence, including p16INK4a(p16), a cyclin-dependent kinase

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Salech, Felipe, Carol D. SanMartín, Jorge Concha-Cerda, et al. "Senescence Markers in Peripheral Blood Mononuclear Cells in Amnestic Mild Cognitive Impairment and Alzheimer’s Disease." International Journal of Molecular Sciences 23, no. 16 (2022): 9387. http://dx.doi.org/10.3390/ijms23169387.

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Recent studies suggest that cellular senescence plays a role in Alzheimer’s Disease (AD) pathogenesis. We hypothesize that cellular senescence markers might be tracked in the peripheral tissues of AD patients. Senescence hallmarks, including altered metabolism, cell-cycle arrest, DNA damage response (DDR) and senescence secretory associated phenotype (SASP), were measured in peripheral blood mononuclear cells (PBMCs) of healthy controls (HC), amnestic mild cognitive impairment (aMCI) and AD patients. Senescence-associated βeta-galactosidase (SA-β-Gal) activity, G0-G1 phase cell-cycle arrest, p

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Zhou, Lin, Jarin Snyder, Katherine C. Murphy, et al. "Abstract A028: Dissecting the role of cellular senescence in prostate cancer initiation and immune suppression." Cancer Research 83, no. 11_Supplement (2023): A028. http://dx.doi.org/10.1158/1538-7445.prca2023-a028.

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Abstract Prostate cancer is the most common malignancy and the second leading cause of cancer-related death in American men. Although many disease cases remain latent for decades, others progress to malignant prostate cancer with high rates of mortality. The molecular underpinnings driving malignancy are still poorly understood, and there is an urgent need to identify mechanisms and informative biomarkers of disease progression. Using the Pb-Cre+; Ptenfl/fl (CP) mouse model, we and others found that Pten genomic loss, a common occurrence in human prostate cancer, leads to induction of cellular

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Chen, Jian, Jian Wang, Haizheng Liu, Cathy Chang, William J. Boyle, and Jay M. Short. "Abstract 2969: Targeting novel senescence markers by conditionally active biologics eliminates senescence-associated secretory phenotype in in vitro and in vivo models." Cancer Research 84, no. 6_Supplement (2024): 2969. http://dx.doi.org/10.1158/1538-7445.am2024-2969.

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Abstract Clearing senescent cells has been shown to have promising effects against cancer and age-related pathologies in preclinical models as well as early human clinical trials. However, current senescent cell elimination strategies are focused on targets that do not distinguish between hyper-inflamed or SASP senescent cells versus relatively non-inflamed senescent cells. The use of senolytics in the clinic is still limited due to their cytotoxicity to either normal cells or potentially beneficial senescent cells. A more effective senescence cell targeted approach is needed to reduce side ef

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Waters, David W., Michael Schuliga, Prabuddha S. Pathinayake, et al. "A Senescence Bystander Effect in Human Lung Fibroblasts." Biomedicines 9, no. 9 (2021): 1162. http://dx.doi.org/10.3390/biomedicines9091162.

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Idiopathic pulmonary fibrosis (IPF) is a chronic disease characterised by a dense fibrosing of the lung parenchyma. An association between IPF and cellular senescence is well established and several studies now describe a higher abundance of senescent fibroblasts and epithelial cells in the lungs of IPF patients compared with age-matched controls. The cause of this abnormal accumulation of senescent cells is unknown but evidence suggests that, once established, senescence can be transferred from senescent to non-senescent cells. In this study, we investigated whether senescent human lung fibro

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Herrmann, Jaqueline, Milen Babic, Markus Tölle, Kai-Uwe Eckardt, Markus van der Giet, and Mirjam Schuchardt. "A Novel Protocol for Detection of Senescence and Calcification Markers by Fluorescence Microscopy." International Journal of Molecular Sciences 21, no. 10 (2020): 3475. http://dx.doi.org/10.3390/ijms21103475.

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Vascular calcification and stiffening of the arterial wall is a systemic phenomenon that is associated with aging and it can be increased by several risk factors. The underlying mechanisms, especially the pathways of cellular senescence, are under current investigation. Easily manageable in vitro settings help to study the signaling pathways. The experimental setting presented here is based on an in vitro model using rat vascular smooth muscle cells and the detection of senescence and osteoblastic markers via immunofluorescence and RNAscope™. Co-staining of the senescence marker p21, the osteo

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Riordan, Ruben. "Brain Cellular Senescence in Mouse Models of Alzheimer's Disease." Innovation in Aging 5, Supplement_1 (2021): 929. http://dx.doi.org/10.1093/geroni/igab046.3363.

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Abstract Abstract The accumulation of senescent cells contributes to aging pathologies, including neurodegenerative diseases, and its selective removal improves physiological and cognitive function in wild type mice as well as in Alzheimer’s disease (AD) models. AD models recapitulate some, but not all components of disease and do so at different rates. Whether brain cellular senescence is recapitulated in some or all AD models, and whether the emergence of cellular senescence in AD mouse models occurs before or after the expected onset of AD-like cognitive deficits in these models is not yet

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Wicher, Sarah A., Benjamin B. Roos, Jacob J. Teske, Yun Hua Fang, Christina Pabelick, and Y. S. Prakash. "Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle." PLOS ONE 16, no. 7 (2021): e0254710. http://dx.doi.org/10.1371/journal.pone.0254710.

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Lung function declines as people age and their lungs become stiffer. With an increasing elderly population, understanding mechanisms that contribute to these structural and functional changes in the aging lung is important. Part of the aging process is characterized by thicker, more fibrotic airways, and senile emphysema caused by changes in lung parenchyma. There is also senescence, which occurs throughout the body with aging. Here, using human airway smooth muscle (ASM) cells from patients in different age groups, we explored senescence pathways and changes in intracellular calcium signaling

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Chadebech, Philippe, Gwellaouen Bodivit, Gaétana Di Liberto, et al. "Ex Vivo Activation of Red Blood Cell Senescence by Plasma from Sickle-Cell Disease Patients: Correlation between Markers and Adhesion Consequences during Acute Disease Events." Biomolecules 11, no. 7 (2021): 963. http://dx.doi.org/10.3390/biom11070963.

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BACKGROUND: Blood transfusion remains a key treatment for managing occlusive episodes and painful crises in sickle-cell disease (SCD). In that clinical context, red blood cells (RBCs) from donors and transfused to patients, may be affected by plasma components in the recipients’ blood. Senescence lesion markers appear on the red cells after transfusion, shortening the RBC lifespan in circulation. In the specific context of SCD, senescence signals can also trigger the occlusive painful events, typical of the disease. This work follows through our previous data that described a RBC senescence pr

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Casella, Gabriel, Rachel Munk, Kyoung Mi Kim, et al. "Transcriptome signature of cellular senescence." Nucleic Acids Research 47, no. 14 (2019): 7294–305. http://dx.doi.org/10.1093/nar/gkz555.

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Abstract Cellular senescence, an integral component of aging and cancer, arises in response to diverse triggers, including telomere attrition, macromolecular damage and signaling from activated oncogenes. At present, senescent cells are identified by the combined presence of multiple traits, such as senescence-associated protein expression and secretion, DNA damage and β-galactosidase activity; unfortunately, these traits are neither exclusively nor universally present in senescent cells. To identify robust shared markers of senescence, we have performed RNA-sequencing analysis across eight di

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Abdul-Aziz, Amina, Raymond D. Devine, Justin M. Lyberger, et al. "Mass Cytometry as a Tool for Investigating Senescence in Multiple Model Systems." Cells 12, no. 16 (2023): 2045. http://dx.doi.org/10.3390/cells12162045.

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Cellular senescence is a durable cell cycle arrest as a result of the finite proliferative capacity of cells. Senescence responds to both intrinsic and extrinsic cellular stresses, such as aging, mitochondrial dysfunction, irradiation, and chemotherapy. Here, we report on the use of mass cytometry (MC) to analyze multiple model systems and demonstrate MC as a platform for senescence analysis at the single-cell level. We demonstrate changes to p16 expression, cell cycling fraction, and histone tail modifications in several established senescent model systems and using isolated human T cells. In

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Cherif, Hosni, Daniel Bisson, Peter Jarzem, Michael Weber, Jean Ouellet, and Lisbet Haglund. "Curcumin and o-Vanillin Exhibit Evidence of Senolytic Activity in Human IVD Cells In Vitro." Journal of Clinical Medicine 8, no. 4 (2019): 433. http://dx.doi.org/10.3390/jcm8040433.

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Curcumin and o-Vanillin cleared senescent intervertebral disc (IVD) cells and reduced the senescence-associated secretory phenotype (SASP) associated with inflammation and back pain. Cells from degenerate and non-mildly-degenerate human IVD were obtained from organ donors and from patients undergoing surgery for low back pain. Gene expression of senescence and SASP markers was evaluated by RT-qPCR in isolated cells, and protein expression of senescence, proliferation, and apoptotic markers was evaluated by immunocytochemistry (ICC). The expression levels of SASP factors were evaluated by enzym

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Teti, Gabriella, Eleonora Mazzotti, Valentina Gatta, Francesca Chiarini, Maria Laura Alfieri, and Mirella Falconi. "Implication of Cellular Senescence in Osteoarthritis: A Study on Equine Synovial Fluid Mesenchymal Stromal Cells." International Journal of Molecular Sciences 24, no. 4 (2023): 3109. http://dx.doi.org/10.3390/ijms24043109.

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Osteoarthritis (OA) is described as a chronic degenerative disease characterized by the loss of articular cartilage. Senescence is a natural cellular response to stressors. Beneficial in certain conditions, the accumulation of senescent cells has been implicated in the pathophysiology of many diseases associated with aging. Recently, it has been demonstrated that mesenchymal stem/stromal cells isolated from OA patients contain many senescent cells that inhibit cartilage regeneration. However, the link between cellular senescence in MSCs and OA progression is still debated. In this study, we ai

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Schwartz, Rachael E., and Irina M. Conboy. "Non-Intrinsic, Systemic Mechanisms of Cellular Senescence." Cells 12, no. 24 (2023): 2769. http://dx.doi.org/10.3390/cells12242769.

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Cellular senescence is believed to contribute to aging and disease through the activity of secreted factors that promote inflammation, remodel the extracellular matrix, and adversely modify the behavior of non-senescent cells. While the markers and properties of senescent cells are still under investigation, it is postulated that cellular senescence manifests in vivo as the consequence of cellular damage that accumulates and becomes exacerbated with time. Yet, the notions that senescence has a solely intrinsic and time-dependent nature are questioned by the rapid induction of senescence in you

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LaFougere, Christian, Brigitte Gueckel, Helmut Dittmann, et al. "Abstract CT095: Update: a phase 1/2, open-label study to assess safety, tolerability, biodistribution, radiation dosimetry and PET imaging characteristics of [18F]FPyGal in comparison to in-vitro diagnostic for the assessment of senescence in oncological patients (NCT04536454)." Cancer Research 83, no. 8_Supplement (2023): CT095. http://dx.doi.org/10.1158/1538-7445.am2023-ct095.

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Abstract It is well established that senescence of cancer cells can be induced by treatment with classical cytotoxic therapies but also by molecularly targeted therapies or immunotherapies, a phenomenon referred to as therapy induced senescence (TIS). Occurrence of intratumoral senescence harbors broad therapeutic implications and may limit the prognosis of cancer patients, as senescent cells, via their senescence associated secretory phenotype (SASP), can suppress anti-tumor immune responses and may increase the metastatic potential of non-senescent cancer cells. Preclinical data suggest that

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Wang, Zijia, Ying Han, Ying Peng та ін. "Senescent epithelial cells remodel the microenvironment for the progression of oral submucous fibrosis through secreting TGF-β1". PeerJ 11 (19 квітня 2023): e15158. http://dx.doi.org/10.7717/peerj.15158.

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Objectives Cellular senescence is strongly associated with fibrosis and tumorigenesis. However, whether the epithelium of oral submucous fibrosis (OSF) undergoes premature senescence remains unclear. This study investigates the roles of senescent epithelial cells in OSF. Methods The immunohistochemistry and Sudan black B staining were performed to identify epithelium senescence in OSF tissues. Arecoline was used to induce human oral keratinocytes (HOKs) senescence. The cell morphology, senescence-associated β galactosidase activity, cell counting Kit 8, immunofluorescence, quantitative real-ti

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Herman, Allison B., Carlos Anerillas, Sophia C. Harris, et al. "Reduction of lamin B receptor levels by miR-340-5p disrupts chromatin, promotes cell senescence and enhances senolysis." Nucleic Acids Research 49, no. 13 (2021): 7389–405. http://dx.doi.org/10.1093/nar/gkab538.

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Abstract A major stress response influenced by microRNAs (miRNAs) is senescence, a state of indefinite growth arrest triggered by sublethal cell damage. Here, through bioinformatic analysis and experimental validation, we identified miR-340-5p as a novel miRNA that foments cellular senescence. miR-340-5p was highly abundant in diverse senescence models, and miR-340-5p overexpression in proliferating cells rendered them senescent. Among the target mRNAs, miR-340-5p prominently reduced the levels of LBR mRNA, encoding lamin B receptor (LBR). Loss of LBR by ectopic overexpression of miR-340-5p de

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Baboota, Ritesh K., Aidin Rawshani, Laurianne Bonnet, et al. "BMP4 and Gremlin 1 regulate hepatic cell senescence during clinical progression of NAFLD/NASH." Nature Metabolism 4, no. 8 (2022): 1007–21. http://dx.doi.org/10.1038/s42255-022-00620-x.

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AbstractThe role of hepatic cell senescence in human non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) is not well understood. To examine this, we performed liver biopsies and extensive characterization of 58 individuals with or without NAFLD/NASH. Here, we show that hepatic cell senescence is strongly related to NAFLD/NASH severity, and machine learning analysis identified senescence markers, the BMP4 inhibitor Gremlin 1 in liver and visceral fat, and the amount of visceral adipose tissue as strong predictors. Studies in liver cell spheroids made from human st

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Piccinato, Carla A., Andrea L. Sertie, Natália Torres, Mario Ferretti, and Eliane Antonioli. "HighOCT4and Lowp16INK4AExpressions DetermineIn VitroLifespan of Mesenchymal Stem Cells." Stem Cells International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/369828.

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After long-term culture, mesenchymal stem cells alter their biological properties and enter into a state of replicative senescence. Although several classical biomarkers have been used for quantitative assessment of cellular senescence, no hallmark has been proven completely unique to the senescent state in cells. We used bone marrow-derived MSCs (BM-MSCs) from different healthy young donors and anin vitromodel with well-defined senescence end points to identify a set of robust markers that could potentially predict the expansion capacity of MSCs preparations before reaching senescence. For ea

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Prlic, Martin, Jilian Sacks, and Michael Bevan. "Dissociating markers of senescence and protective ability in memory T cells (110.16)." Journal of Immunology 188, no. 1_Supplement (2012): 110.16. http://dx.doi.org/10.4049/jimmunol.188.supp.110.16.

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Abstract A set of surface markers is commonly used to predict the potential of CD8 effector T cells to differentiate into memory cells. Similarly, these surface markers together with TNF family member CD27 are frequently used to predict a memory T cell’s ability to mount a recall response. Expression of these markers changes every time a memory cell is stimulated and repeated stimulation can lead to T cell senescence and loss of memory T cell responsiveness. This is a concern for prime-boost vaccine strategies which repeatedly stimulate T cells to increase memory T cell frequency. The molecula

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Mao, Genxiang, and Xiaogang Xu. "Exosomes Derived From Senescent Cells Promote Cellular Senescence." Innovation in Aging 4, Supplement_1 (2020): 132–33. http://dx.doi.org/10.1093/geroni/igaa057.435.

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Abstract Exosomes are one type of small-cell extracellular vesicles (sEVs), which together with the senescence-associated secretory phenotype (SASP) mainly constitute the senescent microenvironment and perform remotely intercellular communication. However, the effects of senescence on exosomes biosynthesis and secretion and its role in the cell senescence are still obscure. Here, we used human fetal lung diploid fibroblasts (2BS) passaged to PD50 to construct the senescent cells model in vitro, which were confirmed by senescence-related β-galactosidase staining, cell cycle distribution, and in

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Chen, Yu-Hsiu, Xin Zhang, Kuei-Yueh Ko, Ming-Feng Hsueh, and Virginia Byers Kraus. "CBX4 Regulates Replicative Senescence of WI-38 Fibroblasts." Oxidative Medicine and Cellular Longevity 2022 (February 23, 2022): 1–15. http://dx.doi.org/10.1155/2022/5503575.

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Cellular senescence is characterized by cell cycle arrest and senescence-associated secretory phenotypes. Cellular senescence can be caused by various stress stimuli such as DNA damage, oxidative stress, and telomere attrition and is related to several chronic diseases, including atherosclerosis, Alzheimer’s disease, and osteoarthritis. Chromobox homolog 4 (CBX4) has been shown to alleviate cellular senescence in human mesenchymal stem cells and is considered a possible target for senomorphic treatment. Here, we explored whether CBX4 expression is associated with replicative senescence in WI-3

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Jo, Hye-Ram, and Jae-Hoon Jeong. "MicroRNA-Mediated Downregulation of HMGB2 Contributes to Cellular Senescence in Microvascular Endothelial Cells." Cells 11, no. 3 (2022): 584. http://dx.doi.org/10.3390/cells11030584.

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High mobility group box 2 (HMGB2) is a non-histone chromosomal protein involved in various biological processes, including cellular senescence. However, its role in cellular senescence has not been evaluated extensively. To determine the regulatory role and mechanism of HMGB2 in cellular senescence, we performed gene expression analysis, senescence staining, and tube formation assays using young and senescent microvascular endothelial cells (MVECs) after small RNA treatment or HMGB2 overexpression. HMGB2 expression decreased with age and was regulated at the transcriptional level. siRNA-mediat

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Romashkan, Sergei, Henry Chang, and Evan C. Hadley. "National Institute on Aging Workshop: Repurposing Drugs or Dietary Supplements for Their Senolytic or Senomorphic Effects: Considerations for Clinical Trials." Journals of Gerontology: Series A 76, no. 6 (2021): 1144–52. http://dx.doi.org/10.1093/gerona/glab028.

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Abstract Background Cell senescence is implicated in numerous age-related conditions. Drugs and nutritional supplements developed for a variety of purposes kill senescent cells (senolytics) or suppress their secretions (senomorphics). There is interest in repurposing such drugs to treat or prevent age-related diseases. To date, only small-scale preliminary trials have been conducted. Method At a workshop convened by the National Institute on Aging in August 2019, academic, industry, and government scientists reviewed issues for phase II trials of potentially repurposable drugs, or dietary supp

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Xu, Linshan, Yuyang Wang, Jianping Wang, Jianglong Zhai, Li Ren, and Guoying Zhu. "Radiation-Induced Osteocyte Senescence Alters Bone Marrow Mesenchymal Stem Cell Differentiation Potential via Paracrine Signaling." International Journal of Molecular Sciences 22, no. 17 (2021): 9323. http://dx.doi.org/10.3390/ijms22179323.

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Cellular senescence and its senescence-associated secretory phenotype (SASP) are widely regarded as promising therapeutic targets for aging-related diseases, such as osteoporosis. However, the expression pattern of cellular senescence and multiple SASP secretion remains unclear, thus leaving a large gap in the knowledge for a desirable intervention targeting cellular senescence. Therefore, there is a critical need to understand the molecular mechanism of SASP secretion in the bone microenvironment that can ameliorate aging-related degenerative pathologies including osteoporosis. In this study,

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Moimas, Silvia, Francesco Salton, Beata Kosmider, et al. "miR-200 family members reduce senescence and restore idiopathic pulmonary fibrosis type II alveolar epithelial cell transdifferentiation." ERJ Open Research 5, no. 4 (2019): 00138–2019. http://dx.doi.org/10.1183/23120541.00138-2019.

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RationaleAlveolar type II (ATII) cells act as adult stem cells contributing to alveolar type I (ATI) cell renewal and play a major role in idiopathic pulmonary fibrosis (IPF), as supported by familial cases harbouring mutations in genes specifically expressed by these cells. During IPF, ATII cells lose their regenerative potential and aberrantly express pathways contributing to epithelial–mesenchymal transition (EMT). The microRNA miR-200 family is downregulated in IPF, but its effect on human IPF ATII cells remains unproven. We wanted to 1) evaluate the characteristics and transdifferentiatin

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Mullani, Nowsheen, Yevheniia Porozhan, Adèle Mangelinck, et al. "Reduced RNA turnover as a driver of cellular senescence." Life Science Alliance 4, no. 3 (2021): e202000809. http://dx.doi.org/10.26508/lsa.202000809.

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Accumulation of senescent cells is an important contributor to chronic inflammation upon aging. The inflammatory phenotype of senescent cells was previously shown to be driven by cytoplasmic DNA. Here, we propose that cytoplasmic double-stranded RNA has a similar effect. We find that several cell types driven into senescence by different routes share an accumulation of long promoter RNAs and 3′ gene extensions rich in retrotransposon sequences. Accordingly, these cells display increased expression of genes involved in response to double stranded RNA of viral origin downstream of the interferon

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