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senescence associated secretory phenotype

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https://www.readbyqxmd.com/read/29432174/naked-mole-rats-can-undergo-developmental-oncogene-induced-and-dna-damage-induced-cellular-senescence
#1
Yang Zhao, Alexander Tyshkovskiy, Daniel Muñoz-Espín, Xiao Tian, Manuel Serrano, Joao Pedro de Magalhaes, Eviatar Nevo, Vadim N Gladyshev, Andrei Seluanov, Vera Gorbunova
Cellular senescence is an important anticancer mechanism that restricts proliferation of damaged or premalignant cells. Cellular senescence also plays an important role in tissue remodeling during development. However, there is a trade-off associated with cellular senescence as senescent cells contribute to aging pathologies. The naked mole rat (NMR) ( Heterocephalus glaber ) is the longest-lived rodent that is resistant to a variety of age-related diseases. Remarkably, NMRs do not show aging phenotypes until very late stages of their lives...
February 5, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29420297/protein-kinase-d1-mediated-classical-protein-secretory-pathway-regulates-oncogene-ras-induced-senescent-response
#2
Yuanyuan Su, Pengfeng Wang, Hong Shen, Zhaomeng Sun, Chenzhong Xu, Guodong Li, Tanjun Tong, Jun Chen
Senescent cells develop senescence-associated secretory phenotype (SASP) which possesses multiple biological functions via autocrine or paracrine manner. However, the status of the protein kinase D1 (PKD1)-mediated classical protein secretory pathway from trans-Golgi network (TGN) to cell surface during cellular senescence and its role in cellular senescent response remain unknown. Here, we show that the activities or quantities of the critical components of this pathway including PKD1, ADP-ribosylation factor 1 (ARF1), and phosphatidylinositol 4-kinase IIIβ (PI4KIIIβ) at TGN are increased in senescent cells...
February 2, 2018: Journal of Cell Science
https://www.readbyqxmd.com/read/29416593/c-myb-and-c-ebp%C3%AE-regulate-opn-and-other-senescence-associated-secretory-phenotype-factors
#3
Kevin C Flanagan, Elise Alspach, Ermira Pazolli, Shankar Parajuli, Qihao Ren, Laura L Arthur, Roberto Tapia, Sheila A Stewart
Tumorigenesis results from the convergence of cell autonomous mutations and corresponding stromal changes that promote tumor cell growth. Senescent cells, which secrete a plethora of pro-tumorigenic factors termed the senescence-associated secretory phenotype (SASP), play an important role in tumor formation. Investigation into SASP regulation revealed that many but not all SASP factors are subject to NF-kB and p38MAPK regulation. However, many pro-tumorigenic SASP factors, including osteopontin (OPN), are not responsive to these canonical pathways leaving the regulation of these factors an open question...
January 2, 2018: Oncotarget
https://www.readbyqxmd.com/read/29415880/mtor-pathway-activation-drives-lung-cell-senescence-and-emphysema
#4
Amal Houssaini, Marielle Breau, Kanny Kebe, Shariq Abid, Elisabeth Marcos, Larissa Lipskaia, Dominique Rideau, Aurelien Parpaleix, Jin Huang, Valerie Amsellem, Nora Vienney, Pierre Validire, Bernard Maitre, Aya Attwe, Christina Lukas, David Vindrieux, Jorge Boczkowski, Genevieve Derumeaux, Mario Pende, David Bernard, Silke Meiners, Serge Adnot
Chronic obstructive pulmonary disease (COPD) is a highly prevalent and devastating condition for which no curative treatment is available. Exaggerated lung cell senescence may be a major pathogenic factor. Here, we investigated the potential role for mTOR signaling in lung cell senescence and alterations in COPD using lung tissue and derived cultured cells from patients with COPD and from age- and sex-matched control smokers. Cell senescence in COPD was linked to mTOR activation, and mTOR inhibition by low-dose rapamycin prevented cell senescence and inhibited the proinflammatory senescence-associated secretory phenotype...
February 8, 2018: JCI Insight
https://www.readbyqxmd.com/read/29415134/induction-of-a-senescence-like-phenotype-in-cultured-human-fetal-microglia-during-hiv-1-infection
#5
Natalie C Chen, Andrea T Partridge, Ferit Tuzer, Justin Cohen, Timothy Nacarelli, Sonia Navas-Martín, Christian Sell, Claudio Torres, Julio Martín-García
HIV-1 causes premature aging in chronically-infected patients. Despite effective anti-retroviral therapy, around 50% of patients suffer HIV-associated neurocognitive disorders (HAND), which likely potentiate aging-associated neurocognitive decline. Microglia support productive HIV-1 infection in the brain. Elevated markers of cellular senescence, including p53 and p21, have been detected in brain tissues from patients with HAND, but the potential for microglia senescence during HIV-1 infection has not been investigated...
February 5, 2018: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
https://www.readbyqxmd.com/read/29415117/attenuated-macrophage-infiltration-in-glomeruli-of-aged-mice-resulting-in-ameliorated-kidney-injury-in-nephrotoxic-serum-nephritis
#6
Yoshikatsu Kaneko, Takamasa Cho, Yuya Sato, Kei Goto, Suguru Yamamoto, Shin Goto, Michael P Madaio, Ichiei Narita
Senescent cells have deleterious effects on the tissue microenvironment through proinflammatory senescence-associated secretory phenotypes; meanwhile, the onset of glomerulonephritis is predominant in younger adults. To clarify the influence of aging on the onset and development of glomerulonephritis, we used a murine model of antibody-mediated nephritis. Sheep nephrotoxic serum was administered in C57BL/6J mice at 12 weeks (adult) or 18 months old (aged) after pre-immunization with sheep IgG. Depositions of sheep IgG and autologous mouse IgG along the glomerular basement membrane and the serum titer of anti-sheep IgG-specific mouse IgG were similar between adult and aged mice...
February 3, 2018: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
https://www.readbyqxmd.com/read/29412148/ginsenoside-f1-suppresses-astrocytic-senescence-associated-secretory-phenotype
#7
Jingang Hou, Changhao Cui, Sunchang Kim, Changkeun Sung, Chulhee Choi
Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by D-galactose via suppressing p38MAPK-dependent NF-κB activity...
February 2, 2018: Chemico-biological Interactions
https://www.readbyqxmd.com/read/29402901/small-molecule-mdm2-antagonists-attenuate-the-senescence-associated-secretory-phenotype
#8
Christopher D Wiley, Nicholas Schaum, Fatouma Alimirah, Jose Alberto Lopez-Dominguez, Arturo V Orjalo, Gary Scott, Pierre-Yves Desprez, Christopher Benz, Albert R Davalos, Judith Campisi
Processes that have been linked to aging and cancer include an inflammatory milieu driven by senescent cells. Senescent cells lose the ability to divide, essentially irreversibly, and secrete numerous proteases, cytokines and growth factors, termed the senescence-associated secretory phenotype (SASP). Senescent cells that lack p53 tumor suppressor function show an exaggerated SASP, suggesting the SASP is negatively controlled by p53. Here, we show that increased p53 activity caused by small molecule inhibitors of MDM2, which promotes p53 degradation, reduces inflammatory cytokine production by senescent cells...
February 5, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29392820/emerging-roles-of-extracellular-vesicles-in-cellular-senescence-and-aging
#9
REVIEW
Masaki Takasugi
Cellular senescence is a cellular program that prevents the proliferation of cells at risk of neoplastic transformation. On the other hand, age-related accumulation of senescent cells promotes aging at least partially due to the senescence-associated secretory phenotype, whereby cells secrete high levels of inflammatory cytokines, chemokines, and matrix metalloproteinases. Emerging evidence, however, indicates that extracellular vesicles (EVs) are important mediators of the effects of senescent cells on their microenvironment...
February 1, 2018: Aging Cell
https://www.readbyqxmd.com/read/29386135/cellular-senescence-is-induced-by-the-environmental-neurotoxin-paraquat-and-contributes-to-neuropathology-linked-to-parkinson-s-disease
#10
Shankar J Chinta, Georgia Woods, Marco Demaria, Anand Rane, Ying Zou, Amanda McQuade, Subramanian Rajagopalan, Chandani Limbad, David T Madden, Judith Campisi, Julie K Andersen
Exposure to the herbicide paraquat (PQ) is associated with an increased risk of idiopathic Parkinson's disease (PD). Therapies based on PQ's presumed mechanisms of action have not, however, yielded effective disease therapies. Cellular senescence is an anticancer mechanism that arrests proliferation of replication-competent cells and results in a pro-inflammatory senescence-associated secretory phenotype (SASP) capable of damaging neighboring tissues. Here, we demonstrate that senescent cell markers are preferentially present within astrocytes in PD brain tissues...
January 23, 2018: Cell Reports
https://www.readbyqxmd.com/read/29374361/targeting-senescent-cells-in-fibrosis-pathology-paradox-and-practical-considerations
#11
REVIEW
Marissa J Schafer, Andrew J Haak, Daniel J Tschumperlin, Nathan K LeBrasseur
PURPOSE OF THE REVIEW: Senescent cells have the capacity to both effect and limit fibrosis. Senotherapeutics target senescent cells to improve aging conditions. Here, we review the contexts in which senescent cells mediate wound healing and fibrotic pathology and the potential utility of senotherapeutic drugs for treatment of fibrotic disease. RECENT FINDINGS: Multi-action and temporal considerations influence deleterious versus beneficial actions of senescent cells...
January 26, 2018: Current Rheumatology Reports
https://www.readbyqxmd.com/read/29360938/long-term-persistent-organic-pollutants-exposure-induced-telomere-dysfunction-and-senescence-associated-secretary-phenotype
#12
Jinghua Yuan, Yang Liu, Juan Wang, Yuxia Zhao, Keqiu Li, Yaqing Jing, Xiaoning Zhang, Qiang Liu, Xin Geng, Guang Li, Feng Wang
Environmentally persistent organic pollutant (POPs) is the general term for refractory organic compounds that show long-range atmospheric transport, environmental persistence, and bioaccumulation. It has been reported that the accumulation of POPs could lead to cellular DNA damage and adverse effects of on metabolic health. To better understand the mechanism of the health risks associated with POPs, we conducted an evidence based cohort investigation (n=5955) at the Jinghai e-waste disposal center in China from 2009-2016, where people endure serious POPs exposure...
January 19, 2018: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
https://www.readbyqxmd.com/read/29352261/insight-into-the-role-of-pikk-family-members-and-nf-%C3%B0%C2%BAb-in-dnadamage-induced-senescence-and-senescence-associated-secretory-phenotype-of-colon-cancer-cells
#13
Anna Strzeszewska, Olga Alster, Grażyna Mosieniak, Agata Ciolko, Ewa Sikora
Senescence of cancer cells is an important outcome of treatment of many cancer types. Cell senescence is a permanent cell cycle arrest induced by stress conditions, including DNA damage. DNA damage activates DNA damage response (DDR), which involves members of the phosphatidylinositol 3-kinase-related kinase (PIKK) superfamily: protein kinases ATM, ATR, and DNA-PKcs. The so-far collected data indicate that ATM, with its downstream targets CHK2, p53, and p21, is the key protein involved in DDR-dependent senescence...
January 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29348392/rapamycin-prevents-the-intervertebral-disc-degeneration-via-inhibiting-differentiation-and-senescence-of-annulus-fibrosus-cells
#14
Changhong Gao, Bin Ning, Chenglin Sang, Ying Zhang
The effects of bleomycin and rapamycin on cellular senescence and differentiation of rabbit annulus fibrosus stem cells (AFSCs) were investigated using a cell culture model. The results showed that bleomycin induced cellular senescence in AFSCs as evidenced by senescence-associated secretory phenotype. The morphology of AFSCs was changed from cobblestone-like cells to pancake-like cells. The senescence-associated β-galactosidase activity, the protein expression of P16 and P21, and inflammatory-related marker gene levels IL-1β, IL-6, and TNF-α were increased in bleomycin-treated AFSCs in a dose-dependent manner...
January 18, 2018: Aging
https://www.readbyqxmd.com/read/29311642/hsp90-inhibition-alters-the-chemotherapy-driven-rearrangement-of-the-oncogenic-secretome
#15
Simona di Martino, Carla Azzurra Amoreo, Barbara Nuvoli, Rossella Galati, Sabrina Strano, Francesco Facciolo, Gabriele Alessandrini, Harvey I Pass, Gennaro Ciliberto, Giovanni Blandino, Ruggero De Maria, Mario Cioce
Adaptive resistance to therapy is a hallmark of cancer progression. To date, it is not entirely clear how microenvironmental stimuli would mediate emergence of therapy-resistant cell subpopulations, although a rearrangement of the cancer cell secretome following therapy-induced stress can be pivotal for such a process. Here, by using the highly chemoresistant malignant pleural mesothelioma (MPM) as an experimental model, we unveiled a key contribution of the chaperone HSP90 at assisting a chemotherapy-instigated Senescence-Associated-Secretory-Phenotype (SASP)...
January 9, 2018: Oncogene
https://www.readbyqxmd.com/read/29218300/the-dual-role-of-cellular-senescence-in-developing-tumors-and-their-response-to-cancer-therapy
#16
REVIEW
Markus Schosserer, Johannes Grillari, Michael Breitenbach
Cellular senescence describes an irreversible growth arrest characterized by distinct morphology, gene expression pattern, and secretory phenotype. The final or intermediate stages of senescence can be reached by different genetic mechanisms and in answer to different external and internal stresses. It has been maintained in the literature but never proven by clearcut experiments that the induction of senescence serves the evolutionary purpose of protecting the individual from development and growth of cancers...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/29206223/a-model-of-the-onset-of-the-senescence-associated-secretory-phenotype-after-dna-damage-induced-senescence
#17
Patrick Meyer, Pallab Maity, Andre Burkovski, Julian Schwab, Christoph Müssel, Karmveer Singh, Filipa F Ferreira, Linda Krug, Harald J Maier, Meinhard Wlaschek, Thomas Wirth, Hans A Kestler, Karin Scharffetter-Kochanek
Cells and tissues are exposed to stress from numerous sources. Senescence is a protective mechanism that prevents malignant tissue changes and constitutes a fundamental mechanism of aging. It can be accompanied by a senescence associated secretory phenotype (SASP) that causes chronic inflammation. We present a Boolean network model-based gene regulatory network of the SASP, incorporating published gene interaction data. The simulation results describe current biological knowledge. The model predicts different in-silico knockouts that prevent key SASP-mediators, IL-6 and IL-8, from getting activated upon DNA damage...
December 4, 2017: PLoS Computational Biology
https://www.readbyqxmd.com/read/29201428/effect-of-aging-on-the-female-reproductive-function
#18
REVIEW
Koumei Shirasuna, Hisataka Iwata
Aging is a complex biological process that involves the accrual of bodily changes over a long life span. In humans, advanced maternal age is associated with infertility and adverse pregnancy complications. Cellular and organic senescence is hypothesized to contribute to the age-related decline in reproductive function. Accumulating evidence suggests that immune cells play pivotal roles in physiological reproductive function and pregnancy. The concept of "inflammaging" has recently emerged- an age-dependent, low-grade, chronic, and systemic inflammatory state induced by the senescence-associated secretory phenotype (SASP), which is produced by the innate immune, parenchymal, and nonparenchymal cells within the organs...
2017: Contraception and Reproductive Medicine
https://www.readbyqxmd.com/read/29186801/epigenetic-basis-of-cellular-senescence-and-its-implications-in-aging
#19
REVIEW
(no author information available yet)
Cellular senescence is a tumor suppressive response that has become recognized as a major contributor of tissue aging. Senescent cells undergo a stable proliferative arrest that protects against neoplastic transformation, but acquire a secretory phenotype that has long-term deleterious effects. Studies are still unraveling the effector mechanisms that underlie these senescence responses with the goal to identify therapeutic interventions. Such effector mechanisms have been linked to the dramatic remodeling in the epigenetic and chromatin landscape that accompany cellular senescence...
November 24, 2017: Genes
https://www.readbyqxmd.com/read/29184185/cellular-senescence-in-gastrointestinal-diseases-from-pathogenesis-to-therapeutics
#20
REVIEW
Nina Frey, Sascha Venturelli, Lars Zender, Michael Bitzer
Senescence is a durable cell cycle arrest that can be induced in response to various stress factors, such as telomere erosion, DNA damage or the aberrant activation of oncogenes. In addition to its well-established role as a stress response programme, research has revealed important physiological roles of senescence in nondisease settings, such as embryonic development, wound healing, tissue repair and ageing. Senescent cells secrete various cytokines, chemokines, matrix remodelling proteases and growth factors, a phenotype collectively referred to as the senescence-associated secretory phenotype...
February 2018: Nature Reviews. Gastroenterology & Hepatology
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