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https://www.readbyqxmd.com/read/29779019/small-extracellular-vesicles-and-their-mirna-cargo-are-anti-apoptotic-members-of-the-senescence-associated-secretory-phenotype
#1
Lucia Terlecki-Zaniewicz, Ingo Lämmermann, Julie Latreille, Madhusudhan Reddy Bobbili, Vera Pils, Markus Schosserer, Regina Weinmüllner, Hanna Dellago, Susanna Skalicky, Dietmar Pum, Juan Carlos Higareda Almaraz, Marcel Scheideler, Frédérique Morizot, Matthias Hackl, Florian Gruber, Johannes Grillari
Loss of functionality during aging of cells and organisms is caused and accompanied by altered cell-to-cell communication and signalling. One factor thereby is the chronic accumulation of senescent cells and the concomitant senescence-associated secretory phenotype (SASP) that contributes to microenvironment remodelling and a pro-inflammatory status. While protein based SASP factors have been well characterized, little is known about small extracellular vesicles (sEVs) and their miRNA cargo. Therefore, we analysed secretion of sEVs from senescent human dermal fibroblasts and catalogued the therein contained miRNAs...
May 19, 2018: Aging
https://www.readbyqxmd.com/read/29777051/cd36-initiates-the-secretory-phenotype-during-the-establishment-of-cellular-senescence
#2
Mengyang Chong, Tao Yin, Rui Chen, Handan Xiang, Lifeng Yuan, Yi Ding, Christopher C Pan, Zhen Tang, Peter B Alexander, Yinjun Jia, Qi-Jing Li, Xiao-Fan Wang
Cellular senescence is a unique cell fate characterized by stable proliferative arrest and the extensive production and secretion of various inflammatory proteins, a phenomenon known as the senescence-associated secretory phenotype (SASP). The molecular mechanisms responsible for generating a SASP in response to senescent stimuli remain largely obscure. Here, using unbiased gene expression profiling, we discover that the scavenger receptor CD36 is rapidly upregulated in multiple cell types in response to replicative, oncogenic, and chemical senescent stimuli...
May 18, 2018: EMBO Reports
https://www.readbyqxmd.com/read/29760459/gata4-dependent-regulation-of-the-secretory-phenotype-via-mcp-1-underlies-lamin-a-mediated-human-mesenchymal-stem-cell-aging
#3
Jin Young Lee, Kyung-Rok Yu, Byung-Chul Lee, Insung Kang, Jae-Jun Kim, Eui-Jung Jung, Hyung-Sik Kim, Yoojin Seo, Soon Won Choi, Kyung-Sun Kang
Defects in the nuclear lamina occur during physiological aging and as. result of premature aging disorders. Aging is also accompanied by an increase in transcription of genes encoding cytokines and chemokines,. phenomenon known as the senescence-associated secretory phenotype (SASP). Progerin and prelamin. trigger premature senescence and loss of function of human mesenchymal stem cells (hMSCs), but little is known about how defects in nuclear lamin. regulate SASP. Here, we show that both progerin overexpression and ZMPSTE24 depletion induce paracrine senescence, especially through the expression of monocyte chemoattractant protein-1 (MCP-1), in hMSCs...
May 14, 2018: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/29753869/dexamethasone-alleviates-pemetrexed-induced-senescence-in-non-small-cell-lung-cancer
#4
Haiyan Ge, Jun Ke, Nuo Xu, Hongqing Li, Jin Gong, Xiangyang Li, Yuanlin Song, Huili Zhu, Chunxue Bai
Pemetrexed (PEM) is a novel and multi-targeted antifolate used as an antineoplastic agent for non-small cell lung cancer (NSCLC) and pleural mesothelioma. Although glucocorticoid was often used with PEM to reduce toxicity during the chemotherapy, it is not clear yet whether glucocorticoid co-administration could affect PEM efficacy in NSCLC. Here we established NSCLC cell lines and examined the effects of dexamethasone (DEX) on PEM sensitivity in vitro and in xenograft models. DEX co-administration reduced chemotherapy sensitivity to PEM in xenograft models...
May 10, 2018: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/29753087/effects-of-salazosulfapyridine-on-the-profile-of-cell-surface-proteins-revealed-by-biotinylation-of-cell-surface-proteins-and-2-dimentional-electrophoresis
#5
Kazuki Omoteyama, Toshiyuki Sato, Mitsumi Arito, Masaaki Sato, Naoya Suematsu, Manae S Kurokawa, Tomohiro Kato
OBJECTIVE: We investigated effects of salazosulfapyridine (SASP) on the protein profile of cell surface (CS)-proteins of SW982, a human synovial sarcoma cell line, using biotinylation of CS-proteins and 2-dimensional fluorescence difference gel electrophoresis (2D-DIGE). METHODS: SW982 cells were treated with SASP and its metabolites, sulfapyridine (SP) and 5-aminosalicylic acid (5ASA). Then the cells were treated with a membrane-impermeable biotinylating reagent...
May 9, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29744983/expression-of-p16-ink-4a-is-a-biomarker-of-chondrocyte-aging-but-does-not-cause-osteoarthritis
#6
Brian O Diekman, Garrett A Sessions, John A Collins, Anne K Knecht, Susan L Strum, Natalia K Mitin, Cathy S Carlson, Richard F Loeser, Norman E Sharpless
Cellular senescence drives a functional decline of numerous tissues with aging by limiting regenerative proliferation and/or by producing pro-inflammatory molecules known as the senescence-associated secretory phenotype (SASP). The senescence biomarker p16INK 4a is a potent inhibitor of the cell cycle but is not essential for SASP production. Thus, it is unclear whether p16INK 4a identifies senescence in hyporeplicative cells such as articular chondrocytes and whether p16INK 4a contributes to pathologic characteristics of cartilage aging...
May 9, 2018: Aging Cell
https://www.readbyqxmd.com/read/29742391/loss-of-mecp2-leads-to-activation-of-p53-and-neuronal-senescence
#7
Minori Ohashi, Elena Korsakova, Denise Allen, Peiyee Lee, Kai Fu, Benni S Vargas, Jessica Cinkornpumin, Carlos Salas, Jenny C Park, Igal Germanguz, Justin Langerman, Contantinos Chronis, Edward Kuoy, Stephen Tran, Xinshu Xiao, Matteo Pellegrini, Kathrin Plath, William E Lowry
To determine the role for mutations of MECP2 in Rett syndrome, we generated isogenic lines of human induced pluripotent stem cells, neural progenitor cells, and neurons from patient fibroblasts with and without MECP2 expression in an attempt to recapitulate disease phenotypes in vitro. Molecular profiling uncovered neuronal-specific gene expression changes, including induction of a senescence-associated secretory phenotype (SASP) program. Patient-derived neurons made without MECP2 showed signs of stress, including induction of P53, and senescence...
May 8, 2018: Stem Cell Reports
https://www.readbyqxmd.com/read/29731994/trabectedin-modulates-the-senescence-associated-secretory-phenotype-and-promotes-cell-death-in-senescent-tumor-cells-by-targeting-nf-%C3%AE%C2%BAb
#8
Simona Camorani, Laura Cerchia, Monica Fedele, Eugenio Erba, Maurizio D'Incalci, Elvira Crescenzi
Therapy-induced senescence is a major cellular response to chemotherapy in solid tumors. Senescent tumor cells acquire a secretory phenotype, or SASP, and produce pro-inflammatory factors, whose expression is largely under NF-κB transcriptional control. Secreted factors play a positive role in driving antitumor immunity, but also exert negative influences on the microenvironment, and promote tumor growth and metastasis. Moreover, subsets of cancer cells can escape the senescence arrest, driving tumor recurrence after treatments...
April 13, 2018: Oncotarget
https://www.readbyqxmd.com/read/29713514/-social-life-of-senescent-cells-what-is-sasp-and-why-study-it
#9
A V Borodkina, P I Deryabin, A A Giukova, N N Nikolsky
Cellular senescence was first described as a failure of normal human cells to divide indefinitely in culture. Until recently, the emphasis in the study of cell senescence has been focused on the accompanying intracellular processes. The focus of the attention has been on the irreversible growth arrest and two important physiological functions that rely on it: suppression of carcinogenesis due to the proliferation loss of damaged cells, and the acceleration of organism aging due to the deterioration of the tissue repair mechanism with age...
January 2018: Acta Naturae
https://www.readbyqxmd.com/read/29712904/the-senescence-associated-secretory-phenotype-is-potentiated-by-feedforward-regulatory-mechanisms-involving-zscan4-and-tak1
#10
Boyi Zhang, Da Fu, Qixia Xu, Xianling Cong, Chunyan Wu, Xiaoming Zhong, Yushui Ma, Zhongwei Lv, Fei Chen, Liu Han, Min Qian, Y Eugene Chin, Eric W-F Lam, Paul Chiao, Yu Sun
The senescence-associated secretory phenotype (SASP) can be provoked by side effects of therapeutic agents, fueling advanced complications including cancer resistance. However, the intracellular signal network supporting initiation and development of the SASP driven by treatment-induced damage remains unclear. Here we report that the transcription factor Zscan4 is elevated for expression by an ATM-TRAF6-TAK1 axis during the acute DNA damage response and enables a long term SASP in human stromal cells. Further, TAK1 activates p38 and PI3K/Akt/mTOR to support the persistent SASP signaling...
April 30, 2018: Nature Communications
https://www.readbyqxmd.com/read/29695641/oxidative-stress-mediated-senescence-in-mesenchymal-progenitor-cells-causes-the-loss-of-their-fibro-adipogenic-potential-and-abrogates-myoblast-fusion
#11
Hidetoshi Sugihara, Naomi Teramoto, Keitaro Yamanouchi, Takashi Matsuwaki, Masugi Nishihara
Sarcopenia is the age-related loss of skeletal muscle mass and function. Skeletal muscle comprises diverse progenitor cells, including mesenchymal progenitor cells (MPCs), which normally support myogenic cell function but cause a decline in skeletal muscle function after differentiating into fibrous/adipose tissue. Cellular senescence is a form of persistent cell cycle arrest caused by cellular stress, including oxidative stress, and is accompanied by the acquisition of senescence-associated secretory phenotype (SASP)...
April 25, 2018: Aging
https://www.readbyqxmd.com/read/29693219/reduction-of-premature-aging-markers-after-gastric-bypass-surgery-in-morbidly-obese-patients
#12
P J Hohensinner, C Kaun, B Ebenbauer, M Hackl, S Demyanets, D Richter, M Prager, J Wojta, Gersina Rega-Kaun
BACKGROUND: Obesity is considered to be a major comorbidity. Obese patients suffer from an increased proinflammatory state associated with a premature aging phenotype including increased secretion of senescence-associated secretory proteins (SASP) and reduced telomere length. Micro-ribonucleic acids (miRNAs) are non-coding RNA molecules that could modify the post-transcriptional process. Several studies have reported associations between miRNAs and metabolic unhealthy conditions. AIM: To determine if bariatric surgery and the resulting weight loss could reverse the premature aging phenotype...
April 25, 2018: Obesity Surgery
https://www.readbyqxmd.com/read/29691234/drug-induced-senescent-multiple-myeloma-cells-elicit-nk-cell-proliferation-by-direct-or-exosome-mediated-il-15-trans-presentation
#13
Cristiana Borrelli, Biancamaria Ricci, Elisabetta Vulpis, Cinzia Fionda, Maria Rosaria Ricciardi, Maria Teresa Petrucci, Laura Masuelli, Agnese Peri, Marco Cippitelli, Alessandra Zingoni, Angela Santoni, Alessandra Soriani
Treatment of multiple myeloma (MM) cells with sub-lethal doses of genotoxic drugs leads to senescence and results in increased NK cell recognition and effector functions. Herein we demonstrated that doxorubicin- and melphalan-treated senescent cells display increased expression of IL15, a cytokine involved in NK cell activation, proliferation, and maturation. IL15 up-regulation was evident at the mRNA and protein level, both in MM cell lines and malignant plasma cells (PCs) from patients' bone marrow (BM) aspirates...
April 24, 2018: Cancer Immunology Research
https://www.readbyqxmd.com/read/29686666/age-and-age-related-diseases-role-of-inflammation-triggers-and-cytokines
#14
REVIEW
Irene Maeve Rea, David S Gibson, Victoria McGilligan, Susan E McNerlan, H Denis Alexander, Owen A Ross
Cytokine dysregulation is believed to play a key role in the remodeling of the immune system at older age, with evidence pointing to an inability to fine-control systemic inflammation, which seems to be a marker of unsuccessful aging. This reshaping of cytokine expression pattern, with a progressive tendency toward a pro-inflammatory phenotype has been called "inflamm-aging." Despite research there is no clear understanding about the causes of "inflamm-aging" that underpin most major age-related diseases, including atherosclerosis, diabetes, Alzheimer's disease, rheumatoid arthritis, cancer, and aging itself...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29677534/punicalagin-induces-senescent-growth-arrest-in-human-papillary-thyroid-carcinoma-bcpap-cells-via-nf-%C3%AE%C2%BAb-signaling-pathway
#15
Xian Cheng, Xin Yao, Shichen Xu, Jie Pan, Huixin Yu, Jiandong Bao, Haixia Guan, Rongrong Lu, Li Zhang
Papillary thyroid carcinoma (PTC) is the most common endocrine carcinoma. Our previous study revealed that punicalagin (PUN), an active component from pomegranate, triggered autophagic cell death and DNA damage response (DDR) in papillary thyroid carcinoma BCPAP cells. But the detailed anti-cancer mechanisms of punicalagin against PTC still remained to be further explored. DDR activation is a proven cause of cellular senescence, which mediates anti-tumor processes under certain circumstances. In this study, we reported that punicalagin treatment generated a senescent phenotype of BCPAP cells characterized as altered morphology, increased cell granularity and senescence-associated β-galactosidase (SA-β-Gal) staining...
April 17, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29675264/blocking-negative-effects-of-senescence-in-human-skin-fibroblasts-with-a-plant-extract
#16
Ingo Lämmermann, Lucia Terlecki-Zaniewicz, Regina Weinmüllner, Markus Schosserer, Hanna Dellago, André Dargen de Matos Branco, Dominik Autheried, Benjamin Sevcnikar, Lisa Kleissl, Irina Berlin, Frédérique Morizot, Francois Lejeune, Nicola Fuzzati, Sandra Forestier, Alix Toribio, Anaïs Tromeur, Lionel Weinberg, Juan Carlos Higareda Almaraz, Marcel Scheideler, Marion Rietveld, Abdoel El Ghalbzouri, Erwin Tschachler, Florian Gruber, Johannes Grillari
There is increasing evidence that senescent cells are a driving force behind many age-related pathologies and that their selective elimination increases the life- and healthspan of mice. Senescent cells negatively affect their surrounding tissue by losing their cell specific functionality and by secreting a pro-tumorigenic and pro-inflammatory mixture of growth hormones, chemokines, cytokines and proteases, termed the senescence-associated secretory phenotype (SASP). Here we identified an extract from the plant Solidago virgaurea subsp...
2018: NPJ Aging and Mechanisms of Disease
https://www.readbyqxmd.com/read/29675106/overexpression-of-klotho-inhibits-helf-fibroblasts-sasp-related-protumoral-effects-on-non-small-cell-lung-cancer-cells
#17
Bo Chen, Yan Liang, Liben Chen, Yunyan Wei, Yue Li, Weihong Zhao, Jianqing Wu
Lung cancer (LC) is the most common cause of death from cancer worldwide, and it is also a closely aging-related disease. Klotho, a new anti-aging gene, has been proven to play a critical role in regulating aging and the development of age-related diseases including LC. However, whether Klotho is a key link between aging and LC is still unknown. Here we report that Klotho can indirectly inhibit LC growth and development through regulating senescence-associated secretory phenotype (SASP). We found that senescent lung fibroblasts (SLF) can promote production of IL-6 and IL-8, which can be effectively inhibited by overexpressing Klotho...
2018: Journal of Cancer
https://www.readbyqxmd.com/read/29670296/paracrine-roles-of-cellular-senescence-in-promoting-tumourigenesis
#18
REVIEW
Jose Mario Gonzalez-Meljem, John Richard Apps, Helen Christina Fraser, Juan Pedro Martinez-Barbera
Senescent cells activate genetic programmes that irreversibly inhibit cellular proliferation, but also endow these cells with distinctive metabolic and signalling phenotypes. Although senescence has historically been considered a protective mechanism against tumourigenesis, the activities of senescent cells are increasingly being associated with age-related diseases, including cancer. An important feature of senescent cells is the secretion of a vast array of pro-inflammatory cytokines, chemokines, and growth factors collectively known as the senescence-associated secretory phenotype (SASP)...
April 19, 2018: British Journal of Cancer
https://www.readbyqxmd.com/read/29593264/downregulation-of-cytoplasmic-dnases-is-implicated-in-cytoplasmic-dna-accumulation-and-sasp-in-senescent-cells
#19
Akiko Takahashi, Tze Mun Loo, Ryo Okada, Fumitaka Kamachi, Yoshihiro Watanabe, Masahiro Wakita, Sugiko Watanabe, Shimpei Kawamoto, Kenichi Miyata, Glen N Barber, Naoko Ohtani, Eiji Hara
Accumulating evidence indicates that the senescence-associated secretory phenotype (SASP) contributes to many aspects of physiology and disease. Thus, controlling the SASP will have tremendous impacts on our health. However, our understanding of SASP regulation is far from complete. Here, we show that cytoplasmic accumulation of nuclear DNA plays key roles in the onset of SASP. Although both DNase2 and TREX1 rapidly remove the cytoplasmic DNA fragments emanating from the nucleus in pre-senescent cells, the expression of these DNases is downregulated in senescent cells, resulting in the cytoplasmic accumulation of nuclear DNA...
March 28, 2018: Nature Communications
https://www.readbyqxmd.com/read/29590617/regulation-of-cellular-senescence-by-polycomb-chromatin-modifiers-through-distinct-dna-damage-and-histone-methylation-dependent-pathways
#20
Takahiro Ito, Yee Voan Teo, Shane A Evans, Nicola Neretti, John M Sedivy
Polycomb group (PcG) factors maintain facultative heterochromatin and mediate many important developmental and differentiation processes. EZH2, a PcG histone H3 lysine-27 methyltransferase, is repressed in senescent cells. We show here that downregulation of EZH2 promotes senescence through two distinct mechanisms. First, depletion of EZH2 in proliferating cells rapidly initiates a DNA damage response prior to a reduction in the levels of H3K27me3 marks. Second, the eventual loss of H3K27me3 induces p16 (CDKN2A) gene expression independent of DNA damage and potently activates genes of the senescence-associated secretory phenotype (SASP)...
March 27, 2018: Cell Reports
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