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senescence associated secretory phenotype

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https://www.readbyqxmd.com/read/28055114/quantitative-analysis-of-cellular-senescence-in-culture-and-in-vivo
#1
Jing Zhao, Heike Fuhrmann-Stroissnigg, Aditi U Gurkar, Rafael R Flores, Akaitz Dorronsoro, Donna B Stolz, Claudette M St Croix, Laura J Niedernhofer, Paul D Robbins
Cellular senescence refers to the irreversible growth arrest of normally dividing cells in response to various types of stress. Cellular senescence is induced by telomere shortening due to repeated cell division, which causes a DNA damage response, as well as genotoxic, oxidative, and inflammatory stress. Strong mitogenic signaling, such as oncogene activation, also drives cells into a senescent state. Senescent cells express a specific subset of genes, termed the senescence-associated secretory phenotype (SASP), including pro-inflammatory factors, growth factors, and matrix metalloproteinases, which together promote non-cell autonomous, secondary senescence...
January 5, 2017: Current Protocols in Cytometry
https://www.readbyqxmd.com/read/28039358/stromal-senescence-by-prolonged-cdk4-6-inhibition-potentiates-tumor-growth
#2
Xiangnan Guan, Kyle M LaPak, Rebecca C Hennessey, Christina Y Yu, Reena Shakya, Jianying Zhang, Christin E Burd
: Senescent cells within the tumor microenvironment (TME) adopt a pro-inflammatory, senescence-associated secretory phenotype (SASP) that promotes cancer initiation, progression and therapeutic resistance. Here, exposure to Palbociclib (PD-0332991), a CDK4/6 inhibitor, induces senescence and a robust SASP in normal fibroblasts. Senescence caused by prolonged CDK4/6 inhibition is DNA damage-independent and associated with Mdm2 downregulation, whereas the SASP elicited by these cells is largely reliant upon NF-kappaB activation...
December 30, 2016: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28030837/bafilomycin-a1-triggers-proliferative-potential-of-senescent-cancer-cells-in-vitro-and-in-nod-scid-mice
#3
Halina Was, Kamila Barszcz, Joanna Czarnecka, Agata Kowalczyk, Tytus Bernas, Ewelina Uzarowska, Paulina Koza, Agata Klejman, Katarzyna Piwocka, Bozena Kaminska, Eva Sikora
Anticancer therapies that induce DNA damage tend to trigger senescence in cancer cells, a process known as therapy-induced senescence (TIS). Such cells may undergo atypical divisions, thus contributing to tumor re-growth. Accumulation of senescent cancer cells reduces survival of patients after chemotherapy. As senescence interplays with autophagy, a dynamic recycling process, we sought to study whether inhibition of autophagy interferes with divisions of TIS cells. We exposed human colon cancer HCT116 cells to repeated cycles of a chemotherapeutic agent - doxorubicin (doxo) and demonstrated induction of hallmarks of TIS (e...
December 21, 2016: Oncotarget
https://www.readbyqxmd.com/read/28017795/injury-induced-senescence-enables-in%C3%A2-vivo-reprogramming-in-skeletal-muscle
#4
Aurélie Chiche, Isabelle Le Roux, Mathieu von Joest, Hiroshi Sakai, Sabela Búa Aguín, Coralie Cazin, Rana Salam, Laurence Fiette, Olinda Alegria, Patricia Flamant, Shahragim Tajbakhsh, Han Li
In vivo reprogramming is a promising approach for tissue regeneration in response to injury. Several examples of in vivo reprogramming have been reported in a variety of lineages, but some including skeletal muscle have so far proven refractory. Here, we show that acute and chronic injury enables transcription-factor-mediated reprogramming in skeletal muscle. Lineage tracing indicates that this response frequently originates from Pax7+ muscle stem cells. Injury is associated with accumulation of senescent cells, and advanced aging or local irradiation further enhanced in vivo reprogramming, while selective elimination of senescent cells reduced reprogramming efficiency...
December 22, 2016: Cell Stem Cell
https://www.readbyqxmd.com/read/27979832/cellular-senescence-promotes-adverse-effects-of-chemotherapy-and-cancer-relapse
#5
Marco Demaria, Monique N O'Leary, Jianhui Chang, Lijian Shao, Su Liu, Fatouma Alimirah, Kristin Koenig, Catherine Le, Natalia Mitin, Allison M Deal, Shani Alston, Emmeline C Academia, Sumner Kilmarx, Alexis Valdovinos, Boshi Wang, Alain de Bruin, Brian K Kennedy, Simon Melov, Daohong Zhou, Norman E Sharpless, Hyman Muss, Judith Campisi
Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a pro-inflammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating cells non-specifically, often with adverse reactions. In accord with prior work, we show that several chemotherapeutic drugs induce senescence of primary murine and human cells. Using a transgenic mouse that permits tracking and eliminating senescent cells, we show that therapy-induced senescent (TIS) cells persist and contribute to local and systemic inflammation...
December 15, 2016: Cancer Discovery
https://www.readbyqxmd.com/read/27951455/relationship-of-inflammatory-profile-of-elderly-patients-serum-and-senescence-associated-secretory-phenotype-with-human-breast-cancer-cells-proliferation-role-of-il6-il8-ratio
#6
Bertha Alicia Barajas-Gómez, Oscar Rosas-Carrasco, Sandra Lisbeth Morales-Rosales, Gibrán Pedraza Vázquez, Viridiana Yazmín González-Puertos, Teresa Juárez-Cedillo, Jorge Antonio García-Álvarez, Norma Edith López-Diazguerrero, Pablo Damián-Matsumura, Mina Königsberg, Armando Luna-López
Aging is considered a systemic, chronic and low-grade inflammatory state, called "inflammaging", which has been contemplated as a risk factor for cancer development and progression in the elderly population. Cellular senescence is a multifactorial phenomenon of growth arrest and distorted function, which has been recognized as a contributor to aging. Senescent cells have an altered secretion pattern called Senescent Associated Secretory Phenotype (SASP), that comprise a complex mix of factors including cytokines, growth factors, chemokines and matrix metalloproteinases among others...
December 9, 2016: Cytokine
https://www.readbyqxmd.com/read/27931848/human-peripheral-late-exhausted-memory-b-cells-express-a-senescent-associated-secretory-phenotype-and-preferentially-utilize-metabolic-signaling-pathways
#7
Daniela Frasca, Alain Diaz, Maria Romero, Bonnie B Blomberg
The percentage of late/exhausted memory (LM) B cells increases with age and we show here that this is associated with a lower influenza vaccine response. To identify novel contributors to the phenotypic and functional changes observed in aged B cells, we sorted the major peripheral B cell subsets [naïve, IgM memory, switched memory (swIg) and late/exhausted memory (LM)] and determined their percentages in the peripheral blood as well as their level of immune activation by measuring basal levels of expression of multiple senescence-associated secretory phenotype (SASP) markers, such as pro-inflammatory cytokines (TNF-α/IL-6/IL-8), inflammatory micro-RNAs (miRs, miR-155/16/93), cell cycle regulators (p16(INK4))...
January 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/27927801/physiological-aging-links-among-adipose-tissue-dysfunction-diabetes-and-frailty
#8
REVIEW
Michael B Stout, Jamie N Justice, Barbara J Nicklas, James L Kirkland
Advancing age is associated with progressive declines in physiological function that lead to overt chronic disease, frailty, and eventual mortality. Importantly, age-related physiological changes occur in cellularity, insulin-responsiveness, secretory profiles, and inflammatory status of adipose tissue, leading to adipose tissue dysfunction. Although the mechanisms underlying adipose tissue dysfunction are multifactorial, the consequences result in secretion of proinflammatory cytokines and chemokines, immune cell infiltration, an accumulation of senescent cells, and an increase in senescence-associated secretory phenotype (SASP)...
January 2017: Physiology
https://www.readbyqxmd.com/read/27907906/senescent-fibroblast-derived-chemerin-promotes-squamous-cell-carcinoma-migration
#9
Vida Farsam, Abhijit Basu, Martina Gatzka, Nicolai Treiber, Lars A Schneider, Medhanie A Mulaw, Tanja Lucas, Stefan Kochanek, Reinhard Dummer, Mitchell P Levesque, Meinhard Wlaschek, Karin Scharffetter-Kochanek
Aging is associated with a rising incidence of cutaneous squamous cell carcinoma (cSCC), an aggressive skin cancer with the potential for local invasion and metastasis. Acquisition of a senescence-associated secretory phenotype (SASP) in dermal fibroblasts has been postulated to promote skin cancer progression in elderly individuals. The underlying molecular mechanisms are largely unexplored. We show that Chemerin, a previously unreported SASP factor released from senescent human dermal fibroblasts, promotes cSCC cell migration, a key feature driving tumor progression...
November 18, 2016: Oncotarget
https://www.readbyqxmd.com/read/27889642/redox-control-of-senescence-and-age-related-disease
#10
REVIEW
Akshaya Chandrasekaran, Maria Del Pilar Sosa Idelchik, J Andrés Melendez
The signaling networks that drive the aging process, associated functional deterioration, and pathologies has captured the scientific community's attention for decades. While many theories exist to explain the aging process, the production of reactive oxygen species (ROS) provides a signaling link between engagement of cellular senescence and several age-associated pathologies. Cellular senescence has evolved to restrict tumor progression but the accompanying senescence-associated secretory phenotype (SASP) promotes pathogenic pathways...
November 16, 2016: Redox Biology
https://www.readbyqxmd.com/read/27886850/cellular-senescence-and-autophagy-in-the-pathogenesis-of-chronic-obstructive-pulmonary-disease-copd-and-idiopathic-pulmonary-fibrosis-ipf
#11
REVIEW
Kazuyoshi Kuwano, Jun Araya, Hiromichi Hara, Shunsuke Minagawa, Naoki Takasaka, Saburo Ito, Kenji Kobayashi, Katsutoshi Nakayama
Aging is associated with impairments in homeostasis. Although aging and senescence are not equivalent, the number of senescent cells increases with aging. Cellular senescence plays important roles in tissue repair or remodeling, as well as embryonic development. Autophagy is a process of lysosomal self-degradation that maintains a homeostatic balance between the synthesis, degradation, and recycling of cellular proteins. Autophagy diminishes with aging; additionally, accelerated aging can be attributed to reduced autophagy...
November 2016: Respiratory Investigation
https://www.readbyqxmd.com/read/27883166/effect-of-low-dose-rapamycin-on-senescence-markers-and-physical-functioning-in-older-adults-with-coronary-artery-disease-results-of-a-pilot-study
#12
M Singh, M D Jensen, A Lerman, S Kushwaha, C S Rihal, B J Gersh, A Behfar, T Tchkonia, R J Thomas, R J Lennon, L R Keenan, A G Moore, J L Kirkland
Rapamycin, an mTOR inhibitor affects senescence through suppression of senescence-associated secretory phenotype (SASP). We studied the safety and feasibility of low-dose rapamycin and its effect on SASP and frailty in elderly undergoing cardiac rehabilitation (CR). 13 patients; 6 (0.5mg), 6 (1.0mg), and 1 patient received 2mg oral rapamycin (serum rapamycin <6ng/ml) daily for 12 weeks. Median age was 73.9±7.5 years and 12 were men. Serum interleukin-6 decreased (2.6 vs 4.4 pg/ml) and MMP-3 (26 vs 23.5 ng/ml) increased...
2016: Journal of Frailty & Aging
https://www.readbyqxmd.com/read/27881217/erratum-to-from-cell-senescence-to-age-related-diseases-differential-mechanisms-of-action-of-senescence-associated-secretory-phenotypes
#13
Hae-Ok Byun, Young-Kyoung Lee, Jeong-Min Kim, Gyesoon Yoon
No abstract text is available yet for this article.
November 2016: BMB Reports
https://www.readbyqxmd.com/read/27869153/cell-senescence-controlling-the-senescence-associated-secretory-phenotype
#14
Paulina Strzyz
No abstract text is available yet for this article.
November 21, 2016: Nature Reviews. Molecular Cell Biology
https://www.readbyqxmd.com/read/27867017/genomic-amplification-of-fanconi-anemia-complementation-group-a-fanca-in-head-and-neck-squamous-cell-carcinoma-hnscc-cellular-mechanisms-of-radioresistance-and-clinical-relevance
#15
Julia Hess, Kristian Unger, Michael Orth, Ulrike Schötz, Lars Schüttrumpf, Verena Zangen, Igor Gimenez-Aznar, Agata Michna, Ludmila Schneider, Ramona Stamp, Martin Selmansberger, Herbert Braselmann, Ludwig Hieber, Guido A Drexler, Sebastian Kuger, Diana Klein, Verena Jendrossek, Anna A Friedl, Claus Belka, Horst Zitzelsberger, Kirsten Lauber
Radio (chemo) therapy is a crucial treatment modality for head and neck squamous cell carcinoma (HNSCC), but relapse is frequent, and the underlying mechanisms remain largely elusive. Therefore, novel biomarkers are urgently needed. Previously, we identified gains on 16q23-24 to be associated with amplification of the Fanconi anemia A (FancA) gene and to correlate with reduced progression-free survival after radiotherapy. Here, we analyzed the effects of FancA on radiation sensitivity in vitro, characterized the underlying mechanisms, and evaluated their clinical relevance...
February 1, 2017: Cancer Letters
https://www.readbyqxmd.com/read/27856124/enhanced-molecular-aging-in-late-life-depression-the-senescent-associated-secretory-phenotype
#16
Breno Satler Diniz, Charles F Reynolds, Etienne Sibille, Chien-Wei Lin, George Tseng, Francis Lotrich, Howard J Aizenstein, Meryl A Butters
OBJECTIVE: This study aims to investigate whether a systemic molecular pattern associated with aging (senescent-associated secretory phenotype [SASP]) is elevated in adults with late-life depression (LLD), compared with never-depressed elderly comparison participants. DESIGN: Cross-sectional study. PARTICIPANTS: We included 111 older adults (80 with LLD and 31 comparison participants) in this study. MEASUREMENT: A panel of 22 SASP-related proteins was extracted from a previous multiplex protein panel performed in these participants...
January 2017: American Journal of Geriatric Psychiatry
https://www.readbyqxmd.com/read/27849057/cell-senescence-is-an-antiviral-defense-mechanism
#17
Maite Baz-Martínez, Sabela Da Silva-Álvarez, Estefanía Rodríguez, Jorge Guerra, Ahmed El Motiam, Anxo Vidal, Tomás García-Caballero, Miguel González-Barcia, Laura Sánchez, César Muñoz-Fontela, Manuel Collado, Carmen Rivas
Cellular senescence is often considered a protection mechanism triggered by conditions that impose cellular stress. Continuous proliferation, DNA damaging agents or activated oncogenes are well-known activators of cell senescence. Apart from a characteristic stable cell cycle arrest, this response also involves a proinflammatory phenotype known as senescence-associated secretory phenotype (SASP). This, together with the widely known interference with senescence pathways by some oncoviruses, had led to the hypothesis that senescence may also be part of the host cell response to fight virus...
November 16, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27846439/a-new-role-for-oxidative-stress-in-aging-the-accelerated-aging-phenotype-in-sod1-mice-is-correlated-to-increased-cellular-senescence
#18
Yiqiang Zhang, Archana Unnikrishnan, Sathyaseelan S Deepa, Yuhong Liu, Yan Li, Yuji Ikeno, Danuta Sosnowska, Holly Van Remmen, Arlan Richardson
In contrast to other mouse models that are deficient in antioxidant enzymes, mice null for Cu/Zn-superoxide dismutase (Sod1(-/)(-) mice) show a major decrease in lifespan and several accelerated aging phenotypes. The goal of this study was to determine if cell senescence might be a contributing factor in the accelerated aging phenotype observed in the Sod1(-/)(-) mice. We focused on kidney because it is a tissue that has been shown to a significant increase in senescent cells with age. The Sod1(-/)(-) mice are characterized by high levels of DNA oxidation in the kidney, which is attenuated by DR...
November 2, 2016: Redox Biology
https://www.readbyqxmd.com/read/27831553/reed-sternberg-cells-in-hodgkin-s-lymphoma-present-features-of-cellular-senescence
#19
J Gopas, E Stern, U Zurgil, J Ozer, A Ben-Ari, G Shubinsky, A Braiman, R Sinay, J Ezratty, V Dronov, S Balachandran, D Benharroch, E Livneh
Hodgkin's Lymphoma (HL) is one of the most prevailing malignancies in young adults. Reed-Sternberg (RS) cells in HL have distinctive large cell morphology, are characteristic of the disease and their presence is essential for diagnosis. Enlarged cells are one of the hallmarks of senescence, but whether RS cells are senescent has not been previously investigated. Here we show that RS cells have characteristics of senescent cells; RS cells in HL biopsies specifically express the senescence markers and cell cycle inhibitors p21(Cip1) and p16(INK4a) and are negative for the proliferation marker Ki-67, suggesting that these cells have ceased to proliferate...
November 10, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27812882/induction-and-detection-of-oncogene-induced-cellular-senescence-in-drosophila
#20
Mai Nakamura, Tatsushi Igaki
Cellular senescence is induced by various cellular stresses, including activation of the Ras oncogene. In Drosophila imaginal epithelia, clones of cells expressing oncogenic Ras (Ras(V12)) show several markers of cellular senescence, such as elevation of SA-β-gal activity, upregulation of the Cdk inhibitor Dacapo (Dap), and heterochromatinization. However, these cells do not undergo cell cycle arrest or exhibit a DNA damage response (DDR), cellular hypertrophy, or a senescence-associated secretory phenotype (SASP), other essential markers of cellular senescence...
2017: Methods in Molecular Biology
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