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senescence associated secretory phenotype

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https://www.readbyqxmd.com/read/28822679/spatial-and-temporal-control-of-senescence
#1
REVIEW
Yoko Ito, Matthew Hoare, Masashi Narita
Cellular senescence is an autonomous tumor suppressor mechanism leading to stable cell cycle arrest. Senescent cells are highly secretory, driving a range of different functions through the senescence-associated secretory phenotype (SASP). Recent findings have suggested that the composition of the SASP is dynamically and spatially regulated and that the changing composition of the SASP can determine the beneficial and detrimental aspects of the senescence program, tipping the balance to either an immunosuppressive/profibrotic environment or proinflammatory/fibrolytic state...
August 16, 2017: Trends in Cell Biology
https://www.readbyqxmd.com/read/28819455/microvesicles-as-potential-biomarkers-for-the-identification-of-senescence-in-human-mesenchymal-stem-cells
#2
Qian Lei, Teng Liu, Fei Gao, Hui Xie, Li Sun, Aiqi Zhao, Wenxiang Ren, Hao Guo, Liming Zhang, Hongxiang Wang, Zhichao Chen, An-Yuan Guo, Qiubai Li
Senescence in human mesenchymal stem cells (MSCs) not only contributes to organism aging and the development of a variety of diseases but also severely impairs their therapeutic properties as a promising cell therapy. Studies searching for efficient biomarkers that represent cellular senescence have attracted much attention; however, no single marker currently provides an accurate cell-free representation of cellular senescence. Here, we studied characteristics of MSC-derived microvesicles (MSC-MVs) that may reflect the senescence in their parental MSCs...
2017: Theranostics
https://www.readbyqxmd.com/read/28811647/biogenesis-of-pro-senescent-microparticles-by-endothelial-colony-forming-cells-from-premature-neonates-is-driven-by-sirt1-dependent-epigenetic-regulation-of-mkk6
#3
Stéphanie Simoncini, Anne-Line Chateau, Stéphane Robert, Dilyana Todorova, Catherine Yzydorzick, Romaric Lacroix, Isabelle Ligi, Laurence Louis, Richard Bachelier, Umberto Simeoni, Frédérique Magdinier, Françoise Dignat-George, Florence Sabatier
Senescent cells may exert detrimental effect on microenvironment through the secretion of soluble factors and the release of extracellular vesicles, such as microparticles, key actors in ageing and cardiovascular diseases. We previously reported that sirtuin-1 (SIRT1) deficiency drives accelerated senescence and dysfunction of endothelial colony-forming cells (ECFC) in PT neonates. Because preterm birth (PT) increases the risk for cardiovascular diseases during neonatal period as well as at adulthood, we hypothesized that SIRT1 deficiency could control the biogenesis of microparticles as part of a senescence-associated secretory phenotype (SASP) of PT-ECFC and investigated the related molecular mechanisms...
August 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28801702/paeonol-attenuates-aging-mrc-5-cells-and-inhibits-epithelial-mesenchymal-transition-of-premalignant-hacat-cells-induced-by-aging-mrc-5-cell-conditioned-medium
#4
Lihua Yang, Shangping Xing, Kun Wang, Hua Yi, Biaoyan Du
Senescence-associated secretory phenotype (SASP) factors, such as IL-6 and IL-8, are extremely critical in tissue microenvironment. Senescent human fibroblasts facilitate epithelial-mesenchymal transition (EMT) in premalignant epithelial cells mainly through the secretion of SASP factors. Meanwhile, premalignant human HaCaT Keratinocyte (HaCaT) cells as immortal epithelial cells are susceptible to malignant transformation. Paeonol, an herbal phenolic component found in peonies, exerts anti-aging and anti-tumor efficacies, while the molecular mechanisms of paeonol on EMT in premalignant HaCaT cells induced by SASP factors are unclear...
August 12, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28790310/p16-ink4a-deletion-ameliorated-renal-tubulointerstitial-injury-in-a-stress-induced-premature-senescence-model-of-bmi-1-deficiency
#5
Jianliang Jin, Jianguo Tao, Xin Gu, Zhenzhen Yu, Rong Wang, Guoping Zuo, Qing Li, Xianhui Lv, Dengshun Miao
To determine whether p16 (INK4a) deletion ameliorated renal tubulointerstitial injury by inhibiting a senescence-associated secretory phenotype (SASP) in Bmi-1-deficient (Bmi-1 (-/-)) mice, renal phenotypes were compared among 5-week-old Bmi-1 and p16 (INK4a) double-knockout, and Bmi-1 (-/-) and wild-type mice. Fifth-passage renal interstitial fibroblasts (RIFs) from the three groups were analyzed for senescence and proliferation. The effect of Bmi-1 deficiency on epithelial-to-mesenchymal transition (EMT) was examined in Bmi-1-knockdown human renal proximal tubular epithelial (HK2) cells, which were treated with concentrated conditioned medium (CM) from the fifth-passage renal interstitial fibroblasts (RIFs) of above three group mice or with exogenous TGF-β1...
August 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28775044/senolytic-drugs-target%C3%A2-alveolar-epithelial-cell-function-and-attenuate-experimental-lung-fibrosis-ex-vivo
#6
Mareike Lehmann, Martina Korfei, Kathrin Mutze, Stephan Klee, Wioletta Skronska-Wasek, Hani N Alsafadi, Chiharu Ota, Rita Costa, Herbert B Schiller, Michael Lindner, Darcy E Wagner, Andreas Günther, Melanie Königshoff
Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease with poor prognosis and limited therapeutic options. The incidence of IPF increases with age, and ageing-related mechanisms such as cellular senescence have been proposed as pathogenic drivers. The lung alveolar epithelium represents a major site of tissue injury in IPF and senescence of this cell population is probably detrimental to lung repair. However, the potential pathomechanisms of alveolar epithelial cell senescence and the impact of senolytic drugs on senescent lung cells and fibrosis remain unknown...
August 2017: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/28763256/cytokine-profile-of-breast-cell-lines-after-different-radiation-doses
#7
Valentina Bravatà, Luigi Minafra, Giusi Irma Forte, Francesco Paolo Cammarata, Giorgio Russo, Federica Maria Di Maggio, Giuseppa Augello, Domenico Lio, Maria Carla Gilardi
PURPOSE: Ionizing radiation (IR) treatment activates inflammatory processes causing the release of a great amount of molecules able to affect the cell survival. The aim of this study was to analyze the cytokine signature of conditioned medium produced by non tumorigenic mammary epithelial cell line MCF10A, as well as MCF7 and MDA-MB-231 breast cancer cell lines, after single high doses of IR in order to understand their role in high radiation response. MATERIAL AND METHODS: We performed a cytokine profile of irradiated conditioned media of MCF10A, MCF7 and MDA-MB-231 cell lines treated with 9 or 23 Gy, by Luminex and ELISA analyses...
August 1, 2017: International Journal of Radiation Biology
https://www.readbyqxmd.com/read/28759028/innate-immune-sensing-of-cytosolic-chromatin-fragments-through-cgas-promotes-senescence
#8
Selene Glück, Baptiste Guey, Muhammet Fatih Gulen, Katharina Wolter, Tae-Won Kang, Niklas Arndt Schmacke, Anne Bridgeman, Jan Rehwinkel, Lars Zender, Andrea Ablasser
Cellular senescence is triggered by various distinct stresses and characterized by a permanent cell cycle arrest. Senescent cells secrete a variety of inflammatory factors, collectively referred to as the senescence-associated secretory phenotype (SASP). The mechanism(s) underlying the regulation of the SASP remains incompletely understood. Here we define a role for innate DNA sensing in the regulation of senescence and the SASP. We find that cyclic GMP-AMP synthase (cGAS) recognizes cytosolic chromatin fragments in senescent cells...
July 31, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28754685/engineering-mammalian-cells-to-seek-senescence-associated-secretory-phenotypes
#9
Anam Qudrat, Janice Wong, Kevin Truong
Since the removal of senescent cells in model organisms has been linked to rejuvenation and increased lifespan, senotherapies have emerged to target senescent cells for death. In particular, interleukin-6 (IL6) is a prominent senescence associated secretory phenotype (SASP) and thus, seeking IL6 could potentially localize engineered cells to senescent cells for therapeutic intervention. Here, we engineered a chimeric IL6 receptor (IL6Rchi) that generates a Ca(2+) signal in response to IL6 stimulation. When IL6Rchi was co-expressed with an engineered Ca(2+)-activated RhoA (CaRQ), it enabled directed migration to IL6 in cells that have no such natural ability...
July 28, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28741506/sasp-tumor-suppressor-or-promoter-yes
#10
REVIEW
Sonia G Rao, James G Jackson
Cellular senescence is a permanent growth arrest in cells with damage or stress that could lead to transformation. Some tumor cells also undergo senescence in response to chemotherapy. Senescent cells secrete cytokines and other factors of the senescence-associated secretory phenotype (SASP) that contribute to tumor suppression by enforcing arrest and recruiting immune cells that remove these damaged or oncogene-expressing cells from organisms. However, some cells can develop a SASP comprising factors that are immunosuppressive and protumorigenic by paracrine mechanisms...
November 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28726780/foxq1-regulates-senescence-associated-inflammation-via-activation-of-sirt1-expression
#11
Pan Wang, Cuicui Lv, Tao Zhang, Junling Liu, Jin Yang, Fangxia Guan, Tianpei Hong
Cellular senescence is an initial barrier to tumor development that prevents the proliferation of premalignant cells. However, some of the features of senescent cells seem to promote tumor progression via senescence-associated secretory phenotype (SASP). Here, we demonstrated that the protein level of forkhead box Q1 (FOXQ1), which highly overexpresses in several kinds of tumors, was significantly downregulated during both replicative and oncogene-induced senescence. Moreover, overexpression of FOXQ1 delayed senescence, whereas FOXQ1 silence led to premature senescence in human fibroblasts...
July 20, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28716705/pathobiology-of-biliary-epithelia
#12
REVIEW
Angela C Cheung, Maria J Lorenzo Pisarello, Nicholas F LaRusso
Cholangiocytes are epithelial cells that line the intra- and extrahepatic biliary tree. They serve predominantly to mediate the content of luminal biliary fluid, which is controlled via numerous signaling pathways influenced by endogenous (e.g., bile acids, nucleotides, hormones, neurotransmitters etc.) and exogenous (microbes/microbial products, drugs etc.) molecules. When injured, cholangiocytes undergo apoptosis/lysis, repair and proliferation. They also become senescent, a form of cell cycle arrest, which may prevent propagation of injury and/or malignant transformation...
July 14, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28701312/inflammation-and-premature-aging-in-advanced-chronic-kidney-disease
#13
Jeroen Kooman, Marijke Dekker, Len A Usvyat, Peter Kotanko, Frank Van der Sande, Casper G Schalkwijk, Paul G Shiels, Peter Stenvinkel
Systemic inflammation in end-stage renal disease (ESRD) is an established risk factor for mortality and a catalyst for other complications which are related to a premature aging phenotype, including muscle wasting, vascular calcification and other forms of premature vascular disease, depression, osteoporosis and frailty. Uremic inflammation is also mechanistically related to mechanisms involved in the aging process, such as telomere shortening, mitochondrial dysfunction, and altered nutrient sensing, which can have direct effect on cellular and tissue function...
July 12, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28699239/analysis-of-individual-cells-identifies-cell-to-cell-variability-following-induction-of-cellular-senescence
#14
Christopher D Wiley, James M Flynn, Christapher Morrissey, Ronald Lebofsky, Joe Shuga, Xiao Dong, Marc A Unger, Jan Vijg, Simon Melov, Judith Campisi
Senescent cells play important roles in both physiological and pathological processes, including cancer and aging. In all cases, however, senescent cells comprise only a small fraction of tissues. Senescent phenotypes have been studied largely in relatively homogeneous populations of cultured cells. In vivo, senescent cells are generally identified by a small number of markers, but whether and how these markers vary among individual cells is unknown. We therefore utilized a combination of single-cell isolation and a nanofluidic PCR platform to determine the contributions of individual cells to the overall gene expression profile of senescent human fibroblast populations...
July 11, 2017: Aging Cell
https://www.readbyqxmd.com/read/28691365/cooperation-between-p21-and-akt-is-required-for-p53-dependent-cellular-senescence
#15
Young Yeon Kim, Hye Jin Jee, Jee-Hyun Um, Young Mi Kim, Sun Sik Bae, Jeanho Yun
Cellular senescence has been implicated in normal aging, tissue homeostasis, and tumor suppression. Although p53 has been shown to be a central mediator of cellular senescence, the signaling pathway by which it induces senescence remains incompletely understood. In this study, we have shown that both Akt and p21 are required to induce cellular senescence in response to p53 expression. In a p53-induced senescence model, we found that Akt activation was essential for inducing a cellular senescence phenotype. Surprisingly, Akt inhibition did not abolish p53-induced cell cycle arrest, but it suppressed the increase in intracellular reactive oxygen species (ROS) levels...
July 9, 2017: Aging Cell
https://www.readbyqxmd.com/read/28687479/senescent-b-cells-in-aging-and-age-related-diseases-their-role-in-the-regulation-of-antibody-responses
#16
REVIEW
Daniela Frasca
Immune cells with a senescence-associated secretory phenotype increase in the blood of elderly individuals or individuals with age-associated diseases or with infections. Although senescent immune cells do not proliferate, they are transcriptionally and metabolically active and affect the microenvironment through the secretion of pro-inflammatory mediators. An age-driven increase in senescent B, T and NK cells has been reported and the function of these cells has been characterized. Results published by different groups have demonstrated that cell senescence induces the accumulation of terminally-differentiated cells characterized by the arrest of cell proliferation but with an active secretory profile which regulates their function through the activation of pathways integrating senescence and energy-sensing signals...
July 4, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28682291/cellular-senescence-what-why-and-how
#17
Matthew J Regulski
Cellular senescence is a process that results from a variety of stresses and leads to a state of irreversible growth arrest. Senescent cells accumulate during aging and have been implicated in promoting a variety of age-related diseases. Cellular senescence may play an important role in tumor suppression, wound healing, and protection against tissue fibrosis; however, accumulating evidence that senescent cells may have harmful effects in vivo and may contribute to tissue remodeling, organismal aging, and many age-related diseases also exists...
June 2017: Wounds: a Compendium of Clinical Research and Practice
https://www.readbyqxmd.com/read/28665427/effects-of-bioactive-compounds-on-senescence-and-components-of-senescence-associated-secretory-phenotypes-in-vitro
#18
REVIEW
Janubová Mária, Žitňanová Ingrid
Senescence is a permanent cell cycle arrest that is accompanied by changes in cell morphology and physiology occurring in vitro and in vivo. Senescence evolved as a beneficial response to damage promoting wound healing, limiting fibrosis, fighting against cancer and helping embryonic development. However, excessive accumulation of senescent cells is considered to play a substantial role in the development of aging-related diseases and other morphological and physiological changes associated with aging. Therefore, the aim of many researchers is to find out a way to eliminate senescent cells and improve the health condition of aging people...
July 19, 2017: Food & Function
https://www.readbyqxmd.com/read/28658729/-senescence-of-the-immune-system-and-alterations-related-with-asthma
#19
Gloria Bertha Vega-Robledo, María Guadalupe Rico-Rosillo
Senescence is an irreversible process by which cells enter to a permanent cell cycle arrest with generalized molecular changes. Senescent cells remain metabolically active and most of them show a secretory phenotype; through its secretion may induce senescence or cancer in other cells. The secretory cells in the so-called transient senescence may participate in embryogenesis, tissue regeneration and immune response. The deleterious changes associated with age affect the immune system members and the immune senescence cause poor response to vaccines and susceptibility to cancer and infections...
April 2017: Revista Alergia Mexico: Organo Oficial de la Sociedad Mexicana de Alergia e Inmunología, A.C
https://www.readbyqxmd.com/read/28649096/-aging-and-homeostasis-aging-of-bone
#20
Seijiro Mori
Quantitative as well as qualitative bone loss occurs with aging in both men and women, leading to alterations in skeletal microarchitecture and increased fracture incidence. Sex steroids, primarily estrogen and testosterone, have been shown to play a central role in the aging process of bone. The relationship between diminishing estrogen levels in women caused by ovarian failure and the development of postmenopausal osteoporosis is widely recognized. Unexpectedly, bone mineral density at various skeletal sites in men is also better correlated with circulating levels of bioavailable estrogen than with testosterone...
2017: Clinical Calcium
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