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senescence associated secretory phenotype

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https://www.readbyqxmd.com/read/29053388/some-chemotherapeutics-treated-colon-cancer-cells-display-a-specific-phenotype-being-a-combination-of-stem-like-and-senescent-cell-features
#1
H Was, J Czarnecka, A Kowalczyk, K Barszcz, T Bernas, K Piwocka, B Kaminska
Colorectal cancer (CRC) is the second leading cause of death among cancer patients in the Northern countries. CRC can reappear a long time after treatment. Recent clinical studies demonstrated that, in response to chemotherapy, cancer cells may undergo stress-induced premature senescence (SIPS), which typically results in growth arrest. Nonetheless, these senescent cells were reported to divide in an atypical manner and thus contribute to cancer re-growth. Therefore, we examined if SIPS escape may follow treatment with chemotherapeutics used clinically: 5-fluorouracil (5-FU), oxaliplatin (OXA) and irinotecan (IRINO)...
October 20, 2017: Cancer Biology & Therapy
https://www.readbyqxmd.com/read/29052866/runx-mediated-growth-arrest-and-senescence-are-attenuated-by-diverse-mechanisms-in-cells-expressing-runx1-fusion-oncoproteins
#2
Gail Anderson, Nancy Mackay, Kathryn Gilroy, Jodie Hay, Gillian Borland, Alma McDonald, Margaret Bell, Siti Ayuni Hassanudin, Ewan Cameron, James C Neil, Anna Kilbey
RUNX gene over-expression inhibits growth of primary cells but transforms cells with tumor suppressor defects, consistent with reported associations with tumor progression. In contrast, chromosomal translocations involving RUNX1 are detectable in utero, suggesting an initiating role in leukemias. How do cells expressing RUNX1 fusion oncoproteins evade RUNX-mediated growth suppression? Previous studies showed that the TEL-RUNX1 fusion from t(12;21) B-ALLs is unable to induce senescence-like growth arrest (SLGA) in primary fibroblasts while potent activity is displayed by the RUNX1-ETO fusion found in t(8;21) AMLs...
October 20, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29045001/anti-inflammaging-effects-of-human-alpha-1-antitrypsin
#3
Ye Yuan, Benedetto DiCiaccio, Ying Li, Ahmed S Elshikha, Denis Titov, Brian Brenner, Lee Seifer, Hope Pan, Nurdina Karic, Mohammad A Akbar, Yuanqing Lu, Sihong Song, Lei Zhou
Inflammaging plays an important role in most age-related diseases. However, the mechanism of inflammaging is largely unknown, and therapeutic control of inflammaging is challenging. Human alpha-1 antitrypsin (hAAT) has immune-regulatory, anti-inflammatory, and cytoprotective properties as demonstrated in several disease models including type 1 diabetes, arthritis, lupus, osteoporosis, and stroke. To test the potential anti-inflammaging effect of hAAT, we generated transgenic Drosophila lines expressing hAAT...
October 17, 2017: Aging Cell
https://www.readbyqxmd.com/read/29044508/differentially-regulated-gene-expression-in-quiescence-vs-senescence-and-identification-of-arid5a-as-a-quiescence-associated-marker
#4
Tarique Anwar, Bijoya Sen, Savera Aggarwal, Rhisita Nath, Ajay Katoch, Mohamed Aiyaz, Nirupma Trehanpati, Sanjeev Khosla, Gayatri Ramakrishna
In multicellular organisms majority of the cells remain in a non-dividing states of either fully differentiated or quiescence (reversible) or senescence (irreversible) conditions. In the present study, gene expression signatures unique to quiescence and senescence were identified using microarray in osteosarcoma cell line, U2OS. Besides, it was also noted that certain genes and pathways like NOD pathway was shared by both the growth arrest conditions. A major highlight of the present study was increased expression of number of chemokines and cytokines in both quiescence and senescence...
October 17, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29024417/human-cd8-emra-t-cells-display-a-senescence-associated-secretory-phenotype-regulated-by-p38-mapk
#5
Lauren A Callender, Elizabeth C Carroll, Robert W J Beal, Emma S Chambers, Sussan Nourshargh, Arne N Akbar, Sian M Henson
Cellular senescence is accompanied by a senescence-associated secretory phenotype (SASP). We show here that primary human senescent CD8(+) T cells also display a SASP comprising chemokines, cytokines and extracellular matrix remodelling proteases that are unique to this subset and contribute to age-associated inflammation. We found the CD8(+) CD45RA(+) CD27(-) EMRA subset to be the most heterogeneous, with a population aligning with the naïve T cells and another with a closer association to the effector memory subset...
October 12, 2017: Aging Cell
https://www.readbyqxmd.com/read/28993289/sirt1-and-parp1-as-epigenome-safeguards-and-micrornas-as-sasp-associated-signals-in-cellular-senescence-and-aging
#6
REVIEW
Seyedhossein Hekmatimoghaddam, Ali Dehghani Firoozabadi, Mohamad Reza Zare-Khormizi, Fatemeh Pourrajab
Cellular senescence (CS) is underlying mechanism of organism aging and is closely interconnected with age-related diseases (ARDs). Thus, any attempt that influences CS, may be undertaken to reverse or inhibit senescence, whereby could prolong healthy life span. Until now, two main proposes are epigenetic and genetic modifications of cell fate. The first one concerns rejuvenation through effective reprogramming in cells undergoing senescence, or derived from very old or progeroid patients, by which is effective in vitro in induced pluripotent stem cells (iPSCs)...
October 6, 2017: Ageing Research Reviews
https://www.readbyqxmd.com/read/28991260/protein-and-chemotherapy-profiling-of-extracellular-vesicles-harvested-from-therapeutic-induced-senescent-triple-negative-breast-cancer-cells
#7
E L Kavanagh, S Lindsay, M Halasz, L C Gubbins, K Weiner-Gorzel, M H Z Guang, A McGoldrick, E Collins, M Henry, A Blanco-Fernández, P O' Gorman, P Fitzpatrick, M J Higgins, P Dowling, A McCann
Triple negative breast cancer (TNBC) is an aggressive subtype with relatively poor clinical outcomes and limited treatment options. Chemotherapy, while killing cancer cells, can result in the generation of highly chemoresistant therapeutic induced senescent (TIS) cells that potentially form stem cell niches resulting in metastases. Intriguingly, senescent cells release significantly more extracellular vesicles (EVs) than non-senescent cells. Our aim was to profile EVs harvested from TIS TNBC cells compared with control cells to identify a potential mechanism by which TIS TNBC cells maintain survival in the face of chemotherapy...
October 9, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28987319/mitochondria-telomeres-and-cell-senescence-implications-for-lung-ageing-and-disease
#8
REVIEW
Jodie Birch, Peter J Barnes, Joao F Passos
Cellular senescence, the irreversible loss of replicative capacity in somatic cells, plays a causal role in the development of age-related pathology and in a number of age-related chronic inflammatory diseases. The ageing lung is marked by an increasing number of senescent cells, and evidence is mounting that senescence may directly contribute to a number of age-related respiratory diseases, including chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). Telomere dysfunction and alterations in mitochondrial homeostasis frequently occur in cellular senescence and are important to the development of the often detrimental senescence-associated secretory phenotype (SASP)...
October 4, 2017: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/28976970/cytoplasmic-chromatin-triggers-inflammation-in-senescence-and-cancer
#9
Zhixun Dou, Kanad Ghosh, Maria Grazia Vizioli, Jiajun Zhu, Payel Sen, Kirk J Wangensteen, Johayra Simithy, Yemin Lan, Yanping Lin, Zhuo Zhou, Brian C Capell, Caiyue Xu, Mingang Xu, Julia E Kieckhaefer, Tianying Jiang, Michal Shoshkes-Carmel, K M Ahasan Al Tanim, Glen N Barber, John T Seykora, Sarah E Millar, Klaus H Kaestner, Benjamin A Garcia, Peter D Adams, Shelley L Berger
Chromatin is traditionally viewed as a nuclear entity that regulates gene expression and silencing. However, we recently discovered the presence of cytoplasmic chromatin fragments that pinch off from intact nuclei of primary cells during senescence, a form of terminal cell-cycle arrest associated with pro-inflammatory responses. The functional significance of chromatin in the cytoplasm is unclear. Here we show that cytoplasmic chromatin activates the innate immunity cytosolic DNA-sensing cGAS-STING (cyclic GMP-AMP synthase linked to stimulator of interferon genes) pathway, leading both to short-term inflammation to restrain activated oncogenes and to chronic inflammation that associates with tissue destruction and cancer...
October 4, 2017: Nature
https://www.readbyqxmd.com/read/28969091/cellular-senescence-senescence-associated-secretory-phenotype-and-chronic-kidney-disease
#10
REVIEW
Wen-Juan Wang, Guang-Yan Cai, Xiang-Mei Chen
Chronic kidney disease (CKD) is increasingly being accepted as a type of renal ageing. The kidney undergoes age-related alterations in both structure and function. To date, a comprehensive analysis of cellular senescence and senescence-associated secretory phenotype (SASP) in CKD is lacking. Hence, this review mainly discusses the relationship between the two phenomena to show the striking similarities between SASP and CKD-associated secretory phenotype (CASP). It has been reported that replicative senescence, stress-induced premature ageing, and epigenetic abnormalities participate in the occurrence and development of CKD...
September 8, 2017: Oncotarget
https://www.readbyqxmd.com/read/28956957/the-potential-of-targeting-sin3b-and-its-associated-complexes-for-cancer-therapy
#11
David J Cantor, Gregory David
Sin3B serves as a scaffold for chromatin-modifying complexes that repress gene transcription to regulate distinct biological processes. Sin3B-containing complexes are critical for cell cycle withdrawal, and abrogation of Sin3B-dependent cell cycle exit impacts tumor progression. Areas covered: In this review, we discuss the biochemical characteristics of Sin3B-containing complexes and explore how these complexes regulate gene transcription. We focus on how Sin3B-containing complexes, through the association of the Rb family of proteins, repress the expression of E2F target genes during quiescence, differentiation, and senescence...
September 28, 2017: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/28921472/telomere-damage-response-and-low-grade-inflammation
#12
Lihui Wang, Xianhua Yu, Jun-Ping Liu
Telomeres at the ends of chromosomes safeguard genome integrity and stability in human nucleated cells. However, telomere repeats shed off during cell proliferation and other stress responses. Our recent studies show that telomere attrition induces not only epithelial stem cell senescence but also low-grade inflammation in the lungs. The senescence-associated low-grade inflammation (SALI) is characteristic of alveolar stem cell replicative senescence, increased proinflammatory and anti-inflammatory cytokines, infiltrated immune cells, and spillover effects...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28916310/dietary-restriction-delays-the-secretion-of-senescence-associated-secretory-phenotype-by-reducing-dna-damage-response-in-the-process-of-renal-aging
#13
Wenjuan Wang, Guangyan Cai, Xiangmei Chen
Dietary restriction (DR) has multiple and essential effects in protecting against DNA damage in model organisms. Persistent DNA damage plays a central role in the process of aging. Senescence-associated secretory phenotype (SASP), as a product of cellular aging, can accelerate the process of cellular senescence as a feedback. In this study, we directly observed whether a DR of 30% for 6months in aged rats could retard SASP by delaying the progression of DNA damage and also found the specific mechanism. The results revealed that a 30% DR could significantly improve renal pathology and some metabolic characteristics...
September 12, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28903474/nitric-oxide-heat-shock-protein-axis-in-menopausal-hot-flushes-neglected-metabolic-issues-of-chronic-inflammatory-diseases-associated-with-deranged-heat-shock-response
#14
Antônio Azambuja Miragem, Paulo Ivo Homem de Bittencourt
BACKGROUND: Although some unequivocal underlying mechanisms of menopausal hot flushes have been demonstrated in animal models, the paucity of similar approaches in humans impedes further mechanistic outcomes. Human studies might show some as yet unexpected physiological mechanisms of metabolic adaptation that permeate the phase of decreased oestrogen levels in both symptomatic and asymptomatic women. This is particularly relevant because both the severity and time span of hot flushes are associated with increased risk of chronic inflammatory disease...
September 1, 2017: Human Reproduction Update
https://www.readbyqxmd.com/read/28894697/the-potential-role-of-senescence-as-a-modulator-of-platelets-and-tumorigenesis
#15
Claudio A Valenzuela, Ricardo Quintanilla, Rodrigo Moore-Carrasco, Nelson E Brown
In addition to thrombus formation, alterations in platelet function are frequently observed in cancer patients. Importantly, both thrombus and tumor formation are influenced by age, although the mechanisms through which physiological aging modulates these processes remain poorly understood. In this context, the potential effects of senescent cells on platelet function represent pathophysiological mechanisms that deserve further exploration. Cellular senescence has traditionally been viewed as a barrier to tumorigenesis...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28894140/d-serine-a-novel-uremic-toxin-induces-senescence-in-human-renal-tubular-cells-via-gcn2-activation
#16
Akira Okada, Masaomi Nangaku, Tzu-Ming Jao, Hiroshi Maekawa, Yu Ishimono, Takahisa Kawakami, Reiko Inagi
The prevalence of chronic kidney disease (CKD), characterized by progressive renal dysfunction with tubulointerstitial fibrosis, is increasing because of societal aging. Uremic toxins, accumulated during renal dysfunction, cause kidney damage, leading to renal deterioration. A recent metabolomic analysis revealed that plasma D-serine accumulation is associated with faster progression of renal dysfunction in CKD patients. However, the causal relationship and the underlying mechanisms remain unclear. Herein, we demonstrated that D-serine markedly induced cellular senescence and apoptosis in a human proximal tubular cell line, HK-2, and primary culture of human renal tubular cells...
September 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28892096/development-and-characterization-of-cholangioids-from-normal-and-diseased-human-cholangiocytes-as-an-in-vitro-model-to-study-primary-sclerosing-cholangitis
#17
Lorena Loarca, Thiago M De Assuncao, Nidhi Jalan-Sakrikar, Steve Bronk, Anuradha Krishnan, Bing Huang, Leslie Morton, Christy Trussoni, Lorena Marcano Bonilla, Eugene Krueger, Steve O'Hara, Patrick Splinter, Guang Shi, María José Lorenzo Pisarello, Gregory J Gores, Robert C Huebert, Nicholas F LaRusso
Primary sclerosing cholangitis (PSC) is an incurable, fibroinflammatory biliary disease for which there is no effective pharmacotherapy. We recently reported cholangiocyte senescence as an important phenotype in PSC while others showed that portal macrophages accumulate in PSC. Unfortunately, our ability to explore cholangiocyte senescence and macrophage accumulation has been hampered by limited in vitro models. Thus, our aim was to develop and characterize a three-dimensional (3D) model of normal and diseased bile ducts (cholangioids) starting with normal human cholangiocytes (NHC), senescent NHC (NHC-sen), and cholangiocytes from PSC patients...
September 11, 2017: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/28891967/ginsenoside-rg3-prevents-oxidative-stress-induced-astrocytic-senescence-and-ameliorates-senescence-paracrine-effects-on-glioblastoma
#18
Jingang Hou, Sunchang Kim, Changkeun Sung, Chulhee Choi
Senescent astrocytes in aging brain express senescence-associated secretory phenotype (SASP) and link with increased brain aging and its related diseases. In order to determine whether ginsenosides ameliorate the astrocytic senescence in vitro, human astrocytic CRT cells and primary rat astrocytes were used in the present study. Ginsenosides Rg1, Re, Rb1 and Rg3 (5 μg/mL) could effectively prevent the astrocytic senescence induced by H₂O₂ exposure. However, these ginsenosides did not reverse the astrocytic senescence...
September 10, 2017: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/28888202/iron-accumulation-in-senescent-cells-is-coupled-with-impaired-ferritinophagy-and-inhibition-of-ferroptosis
#19
Shashank Masaldan, Sharnel A S Clatworthy, Cristina Gamell, Peter M Meggyesy, Antonia-Tonia Rigopoulos, Sue Haupt, Ygal Haupt, Delphine Denoyer, Paul A Adlard, Ashley I Bush, Michael A Cater
Cellular senescence is characterised by the irreversible arrest of proliferation, a pro-inflammatory secretory phenotype and evasion of programmed cell death mechanisms. We report that senescence alters cellular iron acquisition and storage and also impedes iron-mediated cell death pathways. Senescent cells, regardless of stimuli (irradiation, replicative or oncogenic), accumulate vast amounts of intracellular iron (up to 30-fold) with concomitant changes in the levels of iron homeostasis proteins. For instance, ferritin (iron storage) levels provided a robust biomarker of cellular senescence, for associated iron accumulation and for resistance to iron-induced toxicity...
September 1, 2017: Redox Biology
https://www.readbyqxmd.com/read/28878136/old-age-causes-de-novo-intracortical-bone-remodeling-and-porosity-in-mice
#20
Marilina Piemontese, Maria Almeida, Alexander G Robling, Ha-Neui Kim, Jinhu Xiong, Jeff D Thostenson, Robert S Weinstein, Stavros C Manolagas, Charles A O'Brien, Robert L Jilka
Decreased cortical thickness and increased cortical porosity are the key anatomic changes responsible for osteoporotic fractures in elderly women and men. The cellular basis of these changes is unbalanced endosteal and intracortical osteonal remodeling by the osteoclasts and osteoblasts that comprise the basic multicellular units (BMUs). Like humans, mice lose cortical bone with age, but unlike humans, this loss occurs in the face of sex steroid sufficiency. Mice are therefore an ideal model to dissect age-specific osteoporotic mechanisms...
September 7, 2017: JCI Insight
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