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Aging Cell

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https://www.readbyqxmd.com/read/28101970/neuropeptide-y-resists-excess-loss-of-fat-by-lipolysis-in-calorie-restricted-mice-a-trait-potential-for-the-life-extending-effect-of-calorie-restriction
#1
Seongjoon Park, Toshimitsu Komatsu, Sang Eun Kim, Katsuya Tanaka, Hiroko Hayashi, Ryoichi Mori, Isao Shimokawa
Neuropeptide Y (NPY) is an orexigenic peptide that plays an essential role in caloric restriction (CR)-mediated lifespan extension. However, the mechanisms underlying the NPY-mediated effects in CR are poorly defined. Here, we report that NPY deficiency in male mice during CR increases mortality in association with lipodystrophy. NPY(-/-) mice displayed a rapid decrease in body weight and fat mass, as well as increased lipolysis during CR. These alterations in fat regulation were inhibited by the lipolysis inhibitor, acipimox, a treatment associated with reduced mortality...
January 19, 2017: Aging Cell
https://www.readbyqxmd.com/read/28101907/increased-arf-p53-activity-in-stem-cells-aging-and-cancer
#2
REVIEW
Estefania Carrasco-Garcia, Manuel Moreno, Leire Moreno-Cugnon, Ander Matheu
Arf/p53 pathway protects the cells against DNA damage induced by acute stress. This characteristic is the responsible for its tumor suppressor activity. Moreover, it regulates the chronic type of stress associated with aging. This is the basis of its anti-aging activity. Indeed, increased gene dosage of Arf/p53 displays elongated longevity and delayed aging. At a cellular level, it has been recently shown that increased dosage of Arf/p53 delays age-associated stem cell exhaustion and the subsequent decline in tissue homeostasis and regeneration...
January 19, 2017: Aging Cell
https://www.readbyqxmd.com/read/28083909/increased-plekho1-within-osteoblasts-suppresses-smad-dependent-bmp-signaling-to-inhibit-bone-formation-during-aging
#3
Jin Liu, Chao Liang, Baosheng Guo, Xiaohao Wu, Defang Li, Zongkang Zhang, Kang Zheng, Lei Dang, Xiaojuan He, Changwei Lu, Songlin Peng, Xiaohua Pan, Bao-Ting Zhang, Aiping Lu, Ge Zhang
Emerging evidence indicates that the dysregulation of protein ubiquitination plays a crucial role in aging-associated diseases. Smad-dependent canonical BMP signaling pathway is indispensable for osteoblastic bone formation, which could be disrupted by the ubiquitination and subsequent proteasomal degradation of Smad1/5, the key molecules for BMP signaling transduction. However, whether the dysregulation of Smad1/5 ubiquitination and disrupted BMP signaling pathway is responsible for the age-related bone formation reduction is still underexplored...
January 13, 2017: Aging Cell
https://www.readbyqxmd.com/read/28083894/the-amino-acid-transporter-slc36a4-regulates-the-amino-acid-pool-in-retinal-pigmented-epithelial-cells-and-mediates-the-mechanistic-target-of-rapamycin-complex-1-signaling
#4
Peng Shang, Mallika Valapala, Rhonda Grebe, Stacey Hose, Sayan Ghosh, Imran A Bhutto, James T Handa, Gerard A Lutty, Lixia Lu, Jun Wan, Jiang Qian, Yuri Sergeev, Rosa Puertollano, J Samuel Zigler, Guo-Tong Xu, Debasish Sinha
The dry (nonneovascular) form of age-related macular degeneration (AMD), a leading cause of blindness in the elderly, has few, if any, treatment options at present. It is characterized by early accumulation of cellular waste products in the retinal pigmented epithelium (RPE); rejuvenating impaired lysosome function in RPE is a well-justified target for treatment. It is now clear that amino acids and vacuolar-type H(+) -ATPase (V-ATPase) regulate the mechanistic target of rapamycin, complex 1 (mTORC1) signaling in lysosomes...
January 13, 2017: Aging Cell
https://www.readbyqxmd.com/read/28058805/biomarker-signatures-of-aging
#5
Paola Sebastiani, Bharat Thyagarajan, Fangui Sun, Nicole Schupf, Anne B Newman, Monty Montano, Thomas T Perls
Because people age differently, age is not a sufficient marker of susceptibility to disabilities, morbidities, and mortality. We measured nineteen blood biomarkers that include constituents of standard hematological measures, lipid biomarkers, and markers of inflammation and frailty in 4704 participants of the Long Life Family Study (LLFS), age range 30-110 years, and used an agglomerative algorithm to group LLFS participants into clusters thus yielding 26 different biomarker signatures. To test whether these signatures were associated with differences in biological aging, we correlated them with longitudinal changes in physiological functions and incident risk of cancer, cardiovascular disease, type 2 diabetes, and mortality using longitudinal data collected in the LLFS...
January 6, 2017: Aging Cell
https://www.readbyqxmd.com/read/28054425/synergism-between-soluble-guanylate-cyclase-signaling-and-neuropeptides-extends-lifespan-in-the-nematode-caenorhabditis-elegans
#6
Rachel Abergel, Leonid Livshits, Maayan Shaked, Arijit Kumar Chatterjee, Einav Gross
Oxygen (O2 ) homeostasis is important for all aerobic animals. However, the manner by which O2 sensing and homeostasis contribute to lifespan regulation is poorly understood. Here, we use the nematode Caenorhabditis elegans to address this question. We demonstrate that a loss-of-function mutation in the neuropeptide receptor gene npr-1 and a deletion mutation in the atypical soluble guanylate cyclase gcy-35 O2 sensor interact synergistically to extend worm lifespan. The function of npr-1 and gcy-35 in the O2 -sensing neurons AQR, PQR, and URX shortens the lifespan of the worm...
January 4, 2017: Aging Cell
https://www.readbyqxmd.com/read/28035757/papp-a-a-promising-therapeutic-target-for-healthy-longevity
#7
REVIEW
Cheryl A Conover, Claus Oxvig
Pregnancy-associated plasma protein-A (PAPP-A) is a proteolytic enzyme that was discovered to increase local insulin-like growth factor (IGF) availability for receptor activation through cleavage of inhibitory IGF binding proteins (IGFBPs). Reduced IGF signaling has been associated with increased lifespan and healthspan. Therefore, inhibition of PAPP-A represents a novel approach to indirectly decrease the availability of bioactive IGF. Here, we will review data in support of PAPP-A as a therapeutic target to promote healthy longevity...
December 29, 2016: Aging Cell
https://www.readbyqxmd.com/read/28026094/phenotypic-characteristics-of-aged-cd4-cd28-null-t-lymphocytes-are-determined-by-changes-in-the-whole-genome-dna-methylation-pattern
#8
Beatriz Suarez-Álvarez, Ramón M Rodríguez, Karin Schlangen, Aroa Baragaño Raneros, Leonardo Márquez-Kisinousky, Agustín F Fernández, Carmen Díaz-Corte, Ana M Aransay, Carlos López-Larrea
Aging is associated with a progressive loss of the CD28 costimulatory molecule in CD4(+) lymphocytes (CD28(null) T cells), which is accompanied by the acquisition of new biological and functional properties that give rise to an impaired immune response. The regulatory mechanisms that govern the appearance and function of this cell subset during aging and in several associated inflammatory disorders remain controversial. Here, we present the whole-genome DNA methylation and gene expression profiles of CD28(null) T cells and its CD28(+) counterpart...
December 27, 2016: Aging Cell
https://www.readbyqxmd.com/read/28008709/will-you-still-need-me-ca-2-tnt-and-dhpr-will-you-still-cleave-me-calpain-when-i-m-64
#9
José Renato Pinto, Judy Muller-Delp, P Bryant Chase
No abstract text is available yet for this article.
December 23, 2016: Aging Cell
https://www.readbyqxmd.com/read/28000382/aging-impairs-double-strand-break-repair-by-homologous-recombination-in-drosophila-germ-cells
#10
Laetitia Delabaere, Henry A Ertl, Dashiell J Massey, Carolyn M Hofley, Faraz Sohail, Elisa J Bienenstock, Hans Sebastian, Irene Chiolo, Jeannine R LaRocque
Aging is characterized by genome instability, which contributes to cancer formation and cell lethality leading to organismal decline. The high levels of DNA double-strand breaks (DSBs) observed in old cells and premature aging syndromes are likely a primary source of genome instability, but the underlying cause of their formation is still unclear. DSBs might result from higher levels of damage or repair defects emerging with advancing age, but repair pathways in old organisms are still poorly understood. Here, we show that premeiotic germline cells of young and old flies have distinct differences in their ability to repair DSBs by the error-free pathway homologous recombination (HR)...
December 21, 2016: Aging Cell
https://www.readbyqxmd.com/read/27995769/triad3-rnf216-mutations-associated-with-gordon-holmes-syndrome-lead-to-synaptic-and-cognitive-impairments-via-arc-misregulation
#11
Nilofer Husain, Qiang Yuan, Yi-Chun Yen, Olga Pletnikova, Dong Qianying Sally, Paul Worley, Zoë Bichler, H Shawn Je
Multiple loss-of-function mutations in TRIAD3 (a.k.a. RNF216) have recently been identified in patients suffering from Gordon Holmes syndrome (GHS), characterized by cognitive decline, dementia, and movement disorders. TRIAD3A is an E3 ubiquitin ligase that recognizes and facilitates the ubiquitination of its target for degradation by the ubiquitin-proteasome system (UPS). Here, we demonstrate that two of these missense substitutions in TRIAD3 (R660C and R694C) could not regulate the degradation of their neuronal target, activity-regulated cytoskeletal-associated protein (Arc/Arg 3...
December 20, 2016: Aging Cell
https://www.readbyqxmd.com/read/27995756/identification-of-mir-31-5p-mir-141-3p-mir-200c-3p-and-glt1-as-human-liver-aging-markers-sensitive-to-donor-recipient-age-mismatch-in-transplants
#12
Miriam Capri, Fabiola Olivieri, Catia Lanzarini, Daniel Remondini, Vincenzo Borelli, Raffaella Lazzarini, Laura Graciotti, Maria Cristina Albertini, Elena Bellavista, Aurelia Santoro, Fiammetta Biondi, Enrico Tagliafico, Elena Tenedini, Cristina Morsiani, Grazia Pizza, Francesco Vasuri, Antonietta D'Errico, Alessandro Dazzi, Sara Pellegrini, Alessandra Magenta, Marco D'Agostino, Maurizio C Capogrossi, Matteo Cescon, Maria Rita Rippo, Antonio Domenico Procopio, Claudio Franceschi, Gian Luca Grazi
To understand why livers from aged donors are successfully used for transplants, we looked for markers of liver aging in 71 biopsies from donors aged 12-92 years before transplants and in 11 biopsies after transplants with high donor-recipient age-mismatch. We also assessed liver function in 36 age-mismatched recipients. The major findings were the following: (i) miR-31-5p, miR-141-3p, and miR-200c-3p increased with age, as assessed by microRNAs (miRs) and mRNA transcript profiling in 12 biopsies and results were validated by RT-qPCR in a total of 58 biopsies; (ii) telomere length measured by qPCR in 45 samples showed a significant age-dependent shortage; (iii) a bioinformatic approach combining transcriptome and miRs data identified putative miRs targets, the most informative being GLT1, a glutamate transporter expressed in hepatocytes...
December 20, 2016: Aging Cell
https://www.readbyqxmd.com/read/27943596/the-telomere-lengthening-conundrum-it-could-be-biology
#13
Melissa Bateson, Daniel Nettle
Longitudinal studies of human leucocyte telomere length often report a percentage of individuals whose telomeres appear to lengthen. However, based on theoretical considerations and empirical data, Steenstrup et al. (Nucleic Acids Research, 2013, vol 41(13): e131) concluded that this lengthening is unlikely to be a real biological phenomenon and is more likely to be an artefact of measurement error. We dispute the logic underlying this claim. We argue that Steenstrup et al.'s analysis is incomplete because it failed to compare predictions derived from assuming a scenario with no true telomere lengthening with alternative scenarios in which true lengthening occurs...
December 12, 2016: Aging Cell
https://www.readbyqxmd.com/read/27896923/homocysteine-modulates-5-lipoxygenase-expression-level-via-dna-methylation
#14
Jian-Guo Li, Carlos Barrero, Sapna Gupta, Warren D Kruger, Salim Merali, Domenico Praticò
Elevated levels of homocysteinemia (Hcy), a risk factor for late-onset Alzheimer's disease (AD), have been associated with changes in cell methylation. Alzheimer's disease is characterized by an upregulation of the 5-lipoxygenase (5LO), whose promoter is regulated by methylation. However, whether Hcy activates 5LO enzymatic pathway by influencing the methylation status of its promoter remains unknown. Brains from mice with high Hcy were assessed for the 5LO pathway and neuronal cells exposed to Hcy implemented to study the mechanism(s) regulating 5LO expression levels and the effect on amyloid β formation...
November 29, 2016: Aging Cell
https://www.readbyqxmd.com/read/27790859/dimethyl-sulfide-protects-against-oxidative-stress-and-extends-lifespan-via-a-methionine-sulfoxide-reductase-a-dependent-catalytic-mechanism
#15
Xin-Lei Guan, Peng-Fei Wu, Sheng Wang, Juan-Juan Zhang, Zu-Cheng Shen, Han Luo, Hao Chen, Li-Hong Long, Jian-Guo Chen, Fang Wang
Methionine (Met) sulfoxide reductase A (MsrA) is a key endogenous antioxidative enzyme with longevity benefits in animals. Only very few approaches have been reported to enhance MsrA function. Recent reports have indicated that the antioxidant capability of MsrA may involve a Met oxidase activity that facilities the reaction of Met with reactive oxygen species (ROS). Herein, we used a homology modeling approach to search the substrates for the oxidase activity of MsrA. We found that dimethyl sulfide (DMS), a main metabolite that produced by marine algae, emerged as a good substrate for MsrA-catalytic antioxidation...
October 28, 2016: Aging Cell
https://www.readbyqxmd.com/read/27785870/senescence-associated-dna-methylation-is-stochastically-acquired-in-subpopulations-of-mesenchymal-stem-cells
#16
Julia Franzen, Anne Zirkel, Jonathon Blake, Björn Rath, Vladimir Benes, Argyris Papantonis, Wolfgang Wagner
Replicative senescence has a major impact on function and integrity of cell preparations. This process is reflected by continuous DNA methylation (DNAm) changes at specific CpG dinucleotides in the course of in vitro culture, and such modifications can be used to estimate the state of cellular senescence for quality control of cell preparations. Still, it is unclear how senescence-associated DNAm changes are regulated and whether they occur simultaneously across a cell population. In this study, we analyzed global DNAm profiles of human mesenchymal stem cells (MSCs) and human umbilical vein endothelial cells (HUVECs) to demonstrate that senescence-associated DNAm changes are overall similar in these different cell types...
October 26, 2016: Aging Cell
https://www.readbyqxmd.com/read/28090761/modest-overexpression-of-foxo-maintains-cardiac-proteostasis-and-ameliorates-age-associated-functional-decline
#17
Anna C Blice-Baum, Alexander C Zambon, Gaurav Kaushik, Meera C Viswanathan, Adam J Engler, Rolf Bodmer, Anthony Cammarato
Heart performance declines with age. Impaired protein quality control (PQC), due to reduced ubiquitin-proteasome system (UPS) activity, autophagic function, and/or chaperone-mediated protein refolding, contributes to cardiac deterioration. The transcription factor FOXO participates in regulating genes involved in PQC, senescence, and numerous other processes. Here, a comprehensive approach, involving molecular genetics, novel assays to probe insect cardiac physiology, and bioinformatics, was utilized to investigate the influence of heart-restricted manipulation of dFOXO expression in the rapidly aging Drosophila melanogaster model...
February 2017: Aging Cell
https://www.readbyqxmd.com/read/28090760/expression-patterns-of-cardiac-aging-in-drosophila
#18
Leah Cannon, Alexander C Zambon, Anthony Cammarato, Zhi Zhang, Georg Vogler, Matthew Munoz, Erika Taylor, Jérôme Cartry, Sanford I Bernstein, Simon Melov, Rolf Bodmer
Aging causes cardiac dysfunction, often leading to heart failure and death. The molecular basis of age-associated changes in cardiac structure and function is largely unknown. The fruit fly, Drosophila melanogaster, is well-suited to investigate the genetics of cardiac aging. Flies age rapidly over the course of weeks, benefit from many tools to easily manipulate their genome, and their heart has significant genetic and phenotypic similarities to the human heart. Here, we performed a cardiac-specific gene expression study on aging Drosophila and carried out a comparative meta-analysis with published rodent data...
February 2017: Aging Cell
https://www.readbyqxmd.com/read/27730721/lin-28-balances-longevity-and-germline-stem-cell-number-in-caenorhabditis-elegans-through-let-7-akt-daf-16-axis
#19
Dan Wang, Lei Hou, Shuhei Nakamura, Ming Su, Fang Li, Weiyang Chen, Yizhen Yan, Christopher D Green, Di Chen, Hong Zhang, Adam Antebi, Jing-Dong J Han
The RNA-binding protein LIN-28 was first found to control developmental timing in Caenorhabditis elegans. Later, it was found to play important roles in pluripotency, metabolism, and cancer in mammals. Here we report that a low dosage of lin-28 enhanced stress tolerance and longevity, and reduced germline stem/progenitor cell number in C. elegans. The germline LIN-28-regulated microRNA let-7 was required for these effects by targeting akt-1/2 and decreasing their protein levels. AKT-1/2 and the downstream DAF-16 transcription factor were both required for the lifespan and germline stem cell effects of lin-28...
October 11, 2016: Aging Cell
https://www.readbyqxmd.com/read/27723233/distinct-inflammatory-phenotypes-of-microglia-and-monocyte-derived-macrophages-in-alzheimer-s-disease-models-effects-of-aging-and-amyloid-pathology
#20
Elodie Martin, Céline Boucher, Bertrand Fontaine, Cécile Delarasse
Alzheimer's disease (AD) is a neurodegenerative disease characterized by formation of amyloid-β (Aβ) plaques, activated microglia, and neuronal cell death leading to progressive dementia. Recent data indicate that microglia and monocyte-derived macrophages (MDM) are key players in the initiation and progression of AD, yet their respective roles remain to be clarified. As AD occurs mostly in the elderly and aging impairs myeloid functions, we addressed the inflammatory profile of microglia and MDM during aging in TgAPP/PS1 and TgAPP/PS1dE9, two transgenic AD mouse models, compared to WT littermates...
October 8, 2016: Aging Cell
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