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Aging Cell

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https://www.readbyqxmd.com/read/28514055/caveolin-1-deficiency-induces-premature-senescence-with-mitochondrial-dysfunction
#1
Dong-Min Yu, Seung Hee Jung, Hyoung-Tae An, Sungsoo Lee, Jin Hong, Jun Sub Park, Hyun Lee, Hwayeon Lee, Myeong-Suk Bahn, Hyung Chul Lee, Na-Kyung Han, Jesang Ko, Jae-Seon Lee, Young-Gyu Ko
Paradoxical observations have been made regarding the role of caveolin-1 (Cav-1) during cellular senescence. For example, caveolin-1 deficiency prevents reactive oxygen species-induced cellular senescence despite mitochondrial dysfunction, which leads to senescence. To resolve this paradox, we re-addressed the role of caveolin-1 in cellular senescence in human diploid fibroblasts, A549, HCT116, and Cav-1(-/-) mouse embryonic fibroblasts. Cav-1 deficiency (knockout or knockdown) induced cellular senescence via a p53-p21-dependent pathway, downregulating the expression level of the cardiolipin biosynthesis enzymes and then reducing the content of cardiolipin, a critical lipid for mitochondrial respiration...
May 17, 2017: Aging Cell
https://www.readbyqxmd.com/read/28514051/the-ppar%C3%AE-setd8-axis-constitutes-an-epigenetic-p53-independent-checkpoint-on-p21-mediated-cellular-senescence
#2
Chieh-Tien Shih, Yi-Feng Chang, Yi-Tung Chen, Chung-Pei Ma, Hui-Wen Chen, Chang-Ching Yang, Juu-Chin Lu, Yau-Sheng Tsai, Hua-Chien Chen, Bertrand Chin-Ming Tan
Cellular senescence is a permanent proliferative arrest triggered by genome instability or aberrant growth stresses, acting as a protective or even tumor-suppressive mechanism. While several key aspects of gene regulation have been known to program this cessation of cell growth, the involvement of the epigenetic regulation has just emerged but remains largely unresolved. Using a systems approach that is based on targeted gene profiling, we uncovered known and novel chromatin modifiers with putative link to the senescent state of the cells...
May 17, 2017: Aging Cell
https://www.readbyqxmd.com/read/28497576/the-space-where-aging-acts-focus-on-the-gabaergic-synapse
#3
REVIEW
Aleksandra Rozycka, Monika Liguz-Lecznar
As it was established that aging is not associated with massive neuronal loss, as was believed in the mid-20th Century, scientific interest has addressed the influence of aging on particular neuronal subpopulations and their synaptic contacts, which constitute the substrate for neural plasticity. Inhibitory neurons represent the most complex and diverse group of neurons, showing distinct molecular and physiological characteristics and possessing a compelling ability to control the physiology of neural circuits...
May 12, 2017: Aging Cell
https://www.readbyqxmd.com/read/28493459/enhanced-nolc1-promotes-cell-senescence-and-represses-hepatocellular-carcinoma-cell-proliferation-by-disturbing-the-organization-of-nucleolus
#4
Fuwen Yuan, Yu Zhang, Liwei Ma, Qian Cheng, Guodong Li, Tanjun Tong
The nucleolus is a key organelle that is responsible for the synthesis of rRNA and assembly of ribosomal subunits, which is also the center of metabolic control because of the critical role of ribosomes in protein synthesis. Perturbations of rRNA biogenesis are closely related to cell senescence and tumor progression; however, the underlying molecular mechanisms are not well understood. Here, we report that cellular senescence-inhibited gene (CSIG) knockdown up-regulated NOLC1 by stabilizing the 5'UTR of NOLC1 mRNA, and elevated NOLC1 induced the retention of NOG1 in the nucleolus, which is responsible for rRNA processing...
May 10, 2017: Aging Cell
https://www.readbyqxmd.com/read/28474396/mitochondrial-thioredoxin-reductase-2-is-elevated-in-long-lived-primate-as-well-as-rodent-species-and-extends-fly-mean-lifespan
#5
Andrew M Pickering, Marcus Lehr, Christi M Gendron, Scott D Pletcher, Richard A Miller
In a survey of enzymes related to protein oxidation and cellular redox state, we found activity of the redox enzyme thioredoxin reductase (TXNRD) to be elevated in cells from long-lived species of rodents, primates, and birds. Elevated TXNRD activity in long-lived species reflected increases in the mitochondrial form, TXNRD2, rather than the cytosolic forms TXNRD1 and TXNRD3. Analysis of published RNA-Seq data showed elevated TXNRD2 mRNA in multiple organs of longer-lived primates, suggesting that the phenomenon is not limited to skin-derived fibroblasts...
May 5, 2017: Aging Cell
https://www.readbyqxmd.com/read/28455874/quantitative-identification-of-senescent-cells-in-aging-and-disease
#6
Anat Biran, Lior Zada, Paula Abou Karam, Ezra Vadai, Lior Roitman, Yossi Ovadya, Ziv Porat, Valery Krizhanovsky
Senescent cells are present in premalignant lesions and sites of tissue damage and accumulate in tissues with age. In vivo identification, quantification and characterization of senescent cells are challenging tasks that limit our understanding of the role of senescent cells in diseases and aging. Here, we present a new way to precisely quantify and identify senescent cells in tissues on a single-cell basis. The method combines a senescence-associated beta-galactosidase assay with staining of molecular markers for cellular senescence and of cellular identity...
April 28, 2017: Aging Cell
https://www.readbyqxmd.com/read/28449241/autophagy-compensates-impaired-energy-metabolism-in-clpxp-deficient-podospora-anserina-strains-and-extends-healthspan
#7
Laura Knuppertz, Heinz D Osiewacz
The degradation of nonfunctional mitochondrial proteins is of fundamental relevance for maintenance of cellular homeostasis. The heteromeric CLPXP protein complex in the mitochondrial matrix is part of this process. In the fungal aging model Podospora anserina, ablation of CLPXP leads to an increase in healthy lifespan. Here, we report that this counterintuitive increase depends on a functional autophagy machinery. In PaClpXP mutants, autophagy is involved in energy conservation and the compensation of impairments in respiration...
April 27, 2017: Aging Cell
https://www.readbyqxmd.com/read/28436203/endoplasmic-reticulum-proteostasis-impairment-in-aging
#8
REVIEW
Gabriela Martínez, Claudia Duran-Aniotz, Felipe Cabral-Miranda, Juan P Vivar, Claudio Hetz
Perturbed neuronal proteostasis is a salient feature shared by both aging and protein misfolding disorders. The proteostasis network controls the health of the proteome by integrating pathways involved in protein synthesis, folding, trafficking, secretion, and their degradation. A reduction in the buffering capacity of the proteostasis network during aging may increase the risk to undergo neurodegeneration by enhancing the accumulation of misfolded proteins. As almost one-third of the proteome is synthetized at the endoplasmic reticulum (ER), maintenance of its proper function is fundamental to sustain neuronal function...
April 23, 2017: Aging Cell
https://www.readbyqxmd.com/read/28421666/genetic-interplay-between-human-longevity-and-metabolic-pathways-a-large-scale-eqtl-study
#9
Robert Häsler, Geetha Venkatesh, Qihua Tan, Friederike Flachsbart, Anupam Sinha, Philip Rosenstiel, Wolfgang Lieb, Stefan Schreiber, Kaare Christensen, Lene Christiansen, Almut Nebel
Human longevity is a complex phenotype influenced by genetic and environmental components. Unraveling the contribution of genetic vs. nongenetic factors to longevity is a challenging task. Here, we conducted a large-scale RNA-sequencing-based expression quantitative trait loci study (eQTL) with subsequent heritability analysis. The investigation was performed on blood samples from 244 individuals from Germany and Denmark, representing various age groups including long-lived subjects up to the age of 104 years...
April 19, 2017: Aging Cell
https://www.readbyqxmd.com/read/28401731/impact-of-early-personal-history-characteristics-on-the-pace-of-aging-implications-for-clinical-trials-of-therapies-to-slow-aging-and-extend-healthspan
#10
Daniel W Belsky, Avshalom Caspi, Harvey J Cohen, William E Kraus, Sandhya Ramrakha, Richie Poulton, Terrie E Moffitt
Therapies to extend healthspan are poised to move from laboratory animal models to human clinical trials. Translation from mouse to human will entail challenges, among them the multifactorial heterogeneity of human aging. To inform clinical trials about this heterogeneity, we report how humans' pace of biological aging relates to personal-history characteristics. Because geroprotective therapies must be delivered by midlife to prevent age-related disease onset, we studied young-adult members of the Dunedin Study 1972-73 birth cohort (n = 954)...
April 12, 2017: Aging Cell
https://www.readbyqxmd.com/read/28401730/dna-damage-and-senescence-in-osteoprogenitors-expressing-osx1-may-cause-their-decrease-with-age
#11
Ha-Neui Kim, Jianhui Chang, Lijian Shao, Li Han, Srividhya Iyer, Stavros C Manolagas, Charles A O'Brien, Robert L Jilka, Daohong Zhou, Maria Almeida
Age-related bone loss in mice results from a decrease in bone formation and an increase in cortical bone resorption. The former is accounted by a decrease in the number of postmitotic osteoblasts which synthesize the bone matrix and is thought to be the consequence of age-dependent changes in mesenchymal osteoblast progenitors. However, there are no specific markers for these progenitors, and conclusions rely on results from in vitro cultures of mixed cell populations. Moreover, the culprits of such changes remain unknown...
April 12, 2017: Aging Cell
https://www.readbyqxmd.com/read/28401650/caenorhabditis-elegans-orthologs-of-human-genes-differentially-expressed-with-age-are-enriched-for-determinants-of-longevity
#12
George L Sutphin, Grant Backer, Susan Sheehan, Shannon Bean, Caroline Corban, Teresa Liu, Marjolein J Peters, Joyce B J van Meurs, Joanne M Murabito, Andrew D Johnson, Ron Korstanje
We report a systematic RNAi longevity screen of 82 Caenorhabditis elegans genes selected based on orthology to human genes differentially expressed with age. We find substantial enrichment in genes for which knockdown increased lifespan. This enrichment is markedly higher than published genomewide longevity screens in C. elegans and similar to screens that preselected candidates based on longevity-correlated metrics (e.g., stress resistance). Of the 50 genes that affected lifespan, 46 were previously unreported...
April 12, 2017: Aging Cell
https://www.readbyqxmd.com/read/28474484/hyaluronan-keeps-mesenchymal-stem-cells-quiescent-and-maintains-the-differentiation-potential-over-time
#13
Tzyy Yue Wong, Chiung-Hsin Chang, Chen-Hsiang Yu, Lynn L H Huang
Hyaluronan (HA), an abundant polysaccharide found in human bodies, plays a role in the mesenchymal stem cells (MSCs) maintenance. We had previously found that HA prolonged the lifespan, and prevented the cellular aging of murine adipose-derived stromal cells. Recently, we had also summarized the potential pathways associated with HA regulation in human MSCs. In this study, we used the human placenta-derived MSCs (PDMSC) to investigate the effectiveness of HA in maintaining the PDMSC. We found that coating the culture surface coated with 30 μg cm(-2) of HA (C) led to cluster growth of PDMSC, and maintained a higher number of PDMSC in quiescence compared to those grown on the normal tissue culture surface (T)...
June 2017: Aging Cell
https://www.readbyqxmd.com/read/28383136/age-related-decline-in-bubr1-impairs-adult-hippocampal-neurogenesis
#14
Zhongxi Yang, Heechul Jun, Chan-Ii Choi, Ki Hyun Yoo, Chang Hoon Cho, Syed Mohammed Qasim Hussaini, Ambrosia J Simmons, Seonhee Kim, Jan M van Deursen, Darren J Baker, Mi-Hyeon Jang
Aging causes significant declines in adult hippocampal neurogenesis and leads to cognitive disability. Emerging evidence demonstrates that decline in the mitotic checkpoint kinase BubR1 level occurs with natural aging and induces progeroid features in both mice and children with mosaic variegated aneuploidy syndrome. Whether BubR1 contributes to age-related deficits in hippocampal neurogenesis is yet to be determined. Here we report that BubR1 expression is significantly reduced with natural aging in the mouse brain...
June 2017: Aging Cell
https://www.readbyqxmd.com/read/28371268/aging-of-the-skeletal-muscle-extracellular-matrix-drives-a-stem-cell-fibrogenic-conversion
#15
Kristen M Stearns-Reider, Antonio D'Amore, Kevin Beezhold, Benjamin Rothrauff, Loredana Cavalli, William R Wagner, David A Vorp, Alkiviadis Tsamis, Sunita Shinde, Changqing Zhang, Aaron Barchowsky, Thomas A Rando, Rocky S Tuan, Fabrisia Ambrosio
Age-related declines in skeletal muscle regeneration have been attributed to muscle stem cell (MuSC) dysfunction. Aged MuSCs display a fibrogenic conversion, leading to fibrosis and impaired recovery after injury. Although studies have demonstrated the influence of in vitro substrate characteristics on stem cell fate, whether and how aging of the extracellular matrix (ECM) affects stem cell behavior has not been investigated. Here, we investigated the direct effect of the aged muscle ECM on MuSC lineage specification...
June 2017: Aging Cell
https://www.readbyqxmd.com/read/28371119/rapamycin-inhibits-the-secretory-phenotype-of-senescent-cells-by-a-nrf2-independent-mechanism
#16
Rong Wang, Zhen Yu, Bharath Sunchu, James Shoaf, Ivana Dang, Stephanie Zhao, Kelsey Caples, Lynda Bradley, Laura M Beaver, Emily Ho, Christiane V Löhr, Viviana I Perez
Senescent cells contribute to age-related pathology and loss of function, and their selective removal improves physiological function and extends longevity. Rapamycin, an inhibitor of mTOR, inhibits cell senescence in vitro and increases longevity in several species. Nrf2 levels have been shown to decrease with aging and silencing Nrf2 gene induces premature senescence. Therefore, we explored whether Nrf2 is involved in the mechanism by which rapamycin delays cell senescence. In wild-type (WT) mouse fibroblasts, rapamycin increased the levels of Nrf2, and this correlates with the activation of autophagy and a reduction in the induction of cell senescence, as measured by SA-β-galactosidase (β-gal) staining, senescence-associated secretory phenotype (SASP), and p16 and p21 molecular markers...
June 2017: Aging Cell
https://www.readbyqxmd.com/read/28371013/aging-associated-dysregulation-of-homeostatic-immune-response-termination-and-not-initiation
#17
Goutham Pattabiraman, Karol Palasiewicz, John P Galvin, David S Ucker
Immunosenescence is a state of unbalanced immune responsiveness, characterized by a diverse repertoire of seemingly discreet and paradoxical alterations in all aspects of immunity arising in an aging-associated manner. We asked whether aging-associated alterations in the ability of apoptotic cells to elicit immunomodulatory responses (innate apoptotic immunity; IAI) or in IAI responses themselves might underlie the confounding aging-associated anomalies of immunosenescence. We explored this question by examining, as a function of animal age, responsiveness of murine macrophages on the single cell level...
June 2017: Aging Cell
https://www.readbyqxmd.com/read/28345297/residual-cdk1-2-activity-after-dna-damage-promotes-senescence
#18
Erik Müllers, Helena Silva Cascales, Kamila Burdova, Libor Macurek, Arne Lindqvist
In response to DNA damage, a cell can be forced to permanently exit the cell cycle and become senescent. Senescence provides an early barrier against tumor development by preventing proliferation of cells with damaged DNA. By studying single cells, we show that Cdk activity persists after DNA damage until terminal cell cycle exit. This low level of Cdk activity not only allows cell cycle progression, but also promotes cell cycle exit at a decision point in G2 phase. We find that residual Cdk1/2 activity is required for efficient p21 production, allowing for nuclear sequestration of Cyclin B1, subsequent APC/C(C)(dh1) -dependent degradation of mitotic inducers and induction of senescence...
June 2017: Aging Cell
https://www.readbyqxmd.com/read/28317242/chemical-screening-identifies-rock-as-a-target-for-recovering-mitochondrial-function-in-hutchinson-gilford-progeria-syndrome
#19
Hyun Tae Kang, Joon Tae Park, Kobong Choi, Hyo Jei Claudia Choi, Chul Won Jung, Gyu Ree Kim, Young-Sam Lee, Sang Chul Park
Hutchinson-Gilford progeria syndrome (HGPS) constitutes a genetic disease wherein an aging phenotype manifests in childhood. Recent studies indicate that reactive oxygen species (ROS) play important roles in HGPS phenotype progression. Thus, pharmacological reduction in ROS levels has been proposed as a potentially effective treatment for patient with this disorder. In this study, we performed high-throughput screening to find compounds that could reduce ROS levels in HGPS fibroblasts and identified rho-associated protein kinase (ROCK) inhibitor (Y-27632) as an effective agent...
June 2017: Aging Cell
https://www.readbyqxmd.com/read/28317237/disruption-of-the-cx43-mir21-pathway-leads-to-osteocyte-apoptosis-and-increased-osteoclastogenesis-with-aging
#20
Hannah M Davis, Rafael Pacheco-Costa, Emily G Atkinson, Lucas R Brun, Arancha R Gortazar, Julia Harris, Masahiro Hiasa, Surajudeen A Bolarinwa, Toshiyuki Yoneda, Mircea Ivan, Angela Bruzzaniti, Teresita Bellido, Lilian I Plotkin
Skeletal aging results in apoptosis of osteocytes, cells embedded in bone that control the generation/function of bone forming and resorbing cells. Aging also decreases connexin43 (Cx43) expression in bone; and osteocytic Cx43 deletion partially mimics the skeletal phenotype of old mice. Particularly, aging and Cx43 deletion increase osteocyte apoptosis, and osteoclast number and bone resorption on endocortical bone surfaces. We examined herein the molecular signaling events responsible for osteocyte apoptosis and osteoclast recruitment triggered by aging and Cx43 deficiency...
June 2017: Aging Cell
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