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senescence associated secretory phenotype

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https://www.readbyqxmd.com/read/28726780/foxq1-regulates-senescence-associated-inflammation-via-activation-of-sirt1-expression
#1
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
#2
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
#3
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
#4
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
#5
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
#6
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
#7
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
#8
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
#9
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
#10
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
https://www.readbyqxmd.com/read/28647344/oncogene-expressing-senescent-melanocytes-upregulate-mhc-class-ii-a-candidate-melanoma-suppressor-function
#11
John van Tuyn, Farah Jaber-Hijazi, Douglas MacKenzie, John J Cole, Elizabeth Mann, Jeff S Pawlikowski, Taranjit Singh Rai, David M Nelson, Tony McBryan, Andre Ivanov, Karen Blyth, Hong Wu, Simon Milling, Peter D Adams
On acquisition of an oncogenic mutation, primary human and mouse cells can enter oncogene-induced senescence (OIS). OIS is characterized by a stable proliferation arrest and secretion of pro-inflammatory cytokines and chemokines, the senescence-associated secretory phenotype (SASP). Proliferation arrest and the SASP collaborate to enact tumor suppression, the former by blocking cell proliferation and the latter by recruiting immune cells to clear damaged cells. However, the interactions of OIS cells with the immune system are still poorly defined...
June 21, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/28641152/urea-induced-ros-accelerate-senescence-in-endothelial-progenitor-cells
#12
Maria D'Apolito, Anna Laura Colia, Maria Lasalvia, Vito Capozzi, Maria Pia Falcone, Massimo Pettoello-Mantovani, Michael Brownlee, Angela Bruna Maffione, Ida Giardino
BACKGROUND AND AIMS: The pathogenic events responsible for the reduction of endothelial progenitor cell (EPC) number and function seen in patients with chronic renal failure (CRF) are poorly understood. Here we investigate the hypothesis that increased concentrations of urea associated with CRF increase ROS production directly in EPCs, causing abnormalities associated with coronary artery disease risk. METHODS: Human EPCs were isolated from peripheral blood mononuclear cells of healthy donors and cultured in the presence or absence of 20 mmol/L urea...
June 15, 2017: Atherosclerosis
https://www.readbyqxmd.com/read/28613007/transcriptional-coactivator-with-pdz-binding-motif-is-required-to-sustain-testicular-function-on-aging
#13
Mi Gyeong Jeong, Hyuna Song, Ji Hyun Shin, Hana Jeong, Hyo Kyeong Kim, Eun Sook Hwang
Transcriptional coactivator with PDZ-binding motif (TAZ) directly interacts with transcription factors and regulates their transcriptional activity. Extensive functional studies have shown that TAZ plays critical regulatory roles in stem cell proliferation, differentiation, and survival and also modulates the development of organs such as the lung, kidney, heart, and bone. Despite the importance of TAZ in stem cell maintenance, TAZ function has not yet been evaluated in spermatogenic stem cells of the male reproductive system...
June 14, 2017: Aging Cell
https://www.readbyqxmd.com/read/28592031/-the-stimulation-of-human-pulmonary-artery-endothelial-cells-by-cigarette-smoke-extract-contributed-to-cell-senescence-and-induced-human-pulmonary-artery-smooth-cell-migration
#14
L Cai, P C Zhu, Y E Wang, Y T Gao, Q L Ao
Objective: To observe the senescent effect of human pulmonary arterial endothelial cells (HPAEC) stimulated by cigarette smoke extract (CSE) and the effect of secretion of senescent cells on human pulmonary arterial smooth muscles cell (HPASMC) proliferation and migration. Methods: HPAEC was treated with different concentrations of CSE in vitro and cell proliferation was determined by CCK8, senescence cells analyzed by detecting the β-gal activity, and the senescent proteins of cells measured by Western blot...
June 12, 2017: Chinese Journal of Tuberculosis and Respiratory Diseases
https://www.readbyqxmd.com/read/28591504/-cellular-senescence-as-a-common-denominator-in-age-related-diseases
#15
Luis Ángel Maciel-Barón, Viviana I Pérez, Carmen Torres, Viridiana Y González-Puertos, Mina Konigsberg, Norma Edith López-Diazguerrero
Cellular senescence has been traditionally characterized by cell cycle arrest of pot-mitotic cells as a response to a cellular damage. Now is known that senescent cells secret a diverse array of cytokines, chemokines, growth factors and other that altogether are called senescence associates secretory phenotype (SASP), which might have beneficial or deleterious effects on neighbor cells. This review describes those effects as well as the relationship between the SASP and several age related diseases. We also analyze the direction that recent investigations are turning in order to modulate or avoid the effect of the SASP in those pathologies...
July 2017: Revista Médica del Instituto Mexicano del Seguro Social
https://www.readbyqxmd.com/read/28536322/-the-role-of-sasp-in-tumor-microenvironment
#16
Naoko Ohtani
Cellular senescence is a state of irreversible cell proliferation arrest provoked by a persistent DNA damage induced by a variety of potentially oncogenic signals, and it functions as a primary tumor-suppression mechanism. Recent studies, however, revealed that senescent cells have the potential to secrete numerous inflammatory cytokines, chemokines, growth factors and matrix-remodeling factors, since unlike apoptotic cells, senescent cells are viable for a long period of time. This newly identified phenotype of cellular senescence, called senescence-associated secretory phenotype(SASP or senescence-associated secretome), could potentially provide beneficial effects, such as tissue repair, but sometimes could induce deleterious side effects, such as cancer progression, depending on the biological context...
2017: Clinical Calcium
https://www.readbyqxmd.com/read/28533436/metformin-synergizes-with-bcl-xl-bcl-2-inhibitor-abt-263-to-induce-apoptosis-specifically-in-p53-defective-cancer-cells
#17
Xinzhe Li, Bo Li, Zhenhong Ni, Peng Zhou, Bin Wang, Jintao He, Haojun Xiong, Fan Yang, Yaran Wu, Xilin Lyu, Yan Zhang, Yijun Zeng, Jiqin Lian, Fengtian He
p53 deficiency, a frequent event in multiple kinds of malignancies, decreases the sensitivity of diverse targeted chemotherapeutics including the BCL-XL/BCL-2 inhibitor ABT-263. Loss of p53 function can activate mTOR complex 1 (mTORC1), which may make it a vulnerable target. Metformin has shown anti-neoplastic efficiency partially through suppressing mTORC1. However, it remains unknown whether mTORC1 activation confers ABT-263 resistance and whether metformin can overcome it in the p53-defective contexts. In this study, we for the first time demonstrated that metformin and ABT-263 synergistically elicited remarkable apoptosis through orchestrating the pro-apoptotic machineries in various p53-defective cancer cells...
May 22, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28533362/cgas-is-essential-for-cellular-senescence
#18
Hui Yang, Hanze Wang, Junyao Ren, Qi Chen, Zhijian J Chen
Cellular senescence is a natural barrier to tumorigenesis and it contributes to the antitumor effects of several therapies, including radiation and chemotherapeutic drugs. Senescence also plays an important role in aging, fibrosis, and tissue repair. The DNA damage response is a key event leading to senescence, which is characterized by the senescence-associated secretory phenotype (SASP) that includes expression of inflammatory cytokines. Here we show that cGMP-AMP (cGAMP) synthase (cGAS), a cytosolic DNA sensor that activates innate immunity, is essential for senescence...
June 6, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28521866/neovascular-deterioration-impaired-nadph-oxidase-and-inflammatory-cytokine-expression-in-adipose-derived-multipotent-cells-from-subjects-with-metabolic-syndrome
#19
Wilfredo Oliva-Olivera, Said Lhamyani, Leticia Coín-Aragüez, Daniel Castellano-Castillo, Juan Alcaide-Torres, Elena María Yubero-Serrano, Rajaa El Bekay, Francisco José Tinahones
OBJECTIVE: Expansion of adipose tissue depends on the growth of its vascular network and it has been shown that adipose tissue dysfunction in obese subjects with the metabolic syndrome is associated with decreased angiogenesis. However, some subjects with a high body mass index do not develop metabolic abnormalities associated with obesity. In this study we examined the neovascular properties, expression levels of proteins involved in cellular redox balance and inflammatory cytokines in adipose-derived multipotent mesenchymal cells (ASCs) of subjects with different metabolic profiles...
June 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28518126/techniques-to-induce-and-quantify-cellular-senescence
#20
Nicole Noren Hooten, Michele K Evans
In response to cellular stress or damage, proliferating cells can induce a specific program that initiates a state of long-term cell-cycle arrest, termed cellular senescence. Accumulation of senescent cells occurs with organismal aging and through continual culturing in vitro. Senescent cells influence many biological processes, including embryonic development, tissue repair and regeneration, tumor suppression, and aging. Hallmarks of senescent cells include, but are not limited to, increased senescence-associated β-galactosidase activity (SA-β-gal); p16(INK4A), p53, and p21 levels; higher levels of DNA damage, including γ-H2AX; the formation of Senescence-associated Heterochromatin Foci (SAHF); and the acquisition of a Senescence-associated Secretory Phenotype (SASP), a phenomenon characterized by the secretion of a number of pro-inflammatory cytokines and signaling molecules...
May 1, 2017: Journal of Visualized Experiments: JoVE
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