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Aging Cell

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https://www.readbyqxmd.com/read/28625020/methylation-of-the-ribosomal-rna-gene-promoter-is-associated-with-aging-and-age-related-decline
#1
Patrizia D'Aquila, Alberto Montesanto, Maurizio Mandalà, Sabrina Garasto, Vincenzo Mari, Andrea Corsonello, Dina Bellizzi, Giuseppe Passarino
The transcription of ribosomal RNA genes (rDNA) is subject to epigenetic regulation, as it is abrogated by the methylation of CpG dinucleotides within their promoter region. Here, we investigated, through Sequenom platform, the age-related methylation status of the CpG island falling into the rDNA promoter in 472 blood samples from 20- to 105-year-old humans and in different tissues (blood, heart, liver, kidney, and testis) of 15 rats 3-96 weeks old. In humans, we did not find a consistently significant correlation between CpG site methylation and chronological age...
June 17, 2017: Aging Cell
https://www.readbyqxmd.com/read/28620943/drug-repurposing-for-aging-research-using-model-organisms
#2
Matthias Ziehm, Satwant Kaur, Dobril K Ivanov, Pedro J Ballester, David Marcus, Linda Partridge, Janet M Thornton
Many increasingly prevalent diseases share a common risk factor: age. However, little is known about pharmaceutical interventions against aging, despite many genes and pathways shown to be important in the aging process and numerous studies demonstrating that genetic interventions can lead to a healthier aging phenotype. An important challenge is to assess the potential to repurpose existing drugs for initial testing on model organisms, where such experiments are possible. To this end, we present a new approach to rank drug-like compounds with known mammalian targets according to their likelihood to modulate aging in the invertebrates Caenorhabditis elegans and Drosophila...
June 16, 2017: Aging Cell
https://www.readbyqxmd.com/read/28613034/torc1-mediated-sensing-of-chaperone-activity-alters-glucose-metabolism-and-extends-lifespan
#3
Matea Perić, Anita Lovrić, Ana Šarić, Marina Musa, Peter Bou Dib, Marina Rudan, Andrea Nikolić, Sandra Sobočanec, Ana-Matea Mikecin, Sven Dennerlein, Ira Milošević, Kristian Vlahoviček, Nuno Raimundo, Anita Kriško
Protein quality control mechanisms, required for normal cellular functioning, encompass multiple functions related to protein production and maintenance. However, the existence of communication between proteostasis and metabolic networks and its underlying mechanisms remain elusive. Here, we report that enhanced chaperone activity and consequent improved proteostasis are sensed by TORC1 via the activity of Hsp82. Chaperone enrichment decreases the level of Hsp82, which deactivates TORC1 and leads to activation of Snf1/AMPK, regardless of glucose availability...
June 14, 2017: Aging Cell
https://www.readbyqxmd.com/read/28613007/transcriptional-coactivator-with-pdz-binding-motif-is-required-to-sustain-testicular-function-on-aging
#4
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/28612944/the-skn-1-nrf2-transcription-factor-can-protect-against-oxidative-stress-and-increase-lifespan-in-c-%C3%A2-elegans-by-distinct-mechanisms
#5
Jennifer M A Tullet, James W Green, Catherine Au, Alexandre Benedetto, Maximillian A Thompson, Emily Clark, Ann F Gilliat, Adelaide Young, Kathrin Schmeisser, David Gems
In C. elegans, the skn-1 gene encodes a transcription factor that resembles mammalian Nrf2 and activates a detoxification response. skn-1 promotes resistance to oxidative stress (Oxr) and also increases lifespan, and it has been suggested that the former causes the latter, consistent with the theory that oxidative damage causes aging. Here, we report that effects of SKN-1 on Oxr and longevity can be dissociated. We also establish that skn-1 expression can be activated by the DAF-16/FoxO transcription factor, another central regulator of growth, metabolism, and aging...
June 14, 2017: Aging Cell
https://www.readbyqxmd.com/read/28612507/hiv-and-drug-abuse-mediate-astrocyte-senescence-in-a-%C3%AE-catenin-dependent-manner-leading-to-neuronal-toxicity
#6
Chunjiang Yu, Srinivas D Narasipura, Maureen H Richards, Xiu-Ti Hu, Bryan Yamamoto, Lena Al-Harthi
Emerging evidence suggests that cell senescence plays an important role in aging-associated diseases including neurodegenerative diseases. HIV leads to a spectrum of neurologic diseases collectively termed HIV-associated neurocognitive disorders (HAND). Drug abuse, particularly methamphetamine (meth), is a frequently abused psychostimulant among HIV+ individuals and its abuse exacerbates HAND. The mechanism by which HIV and meth lead to brain cell dysregulation is not entirely clear. In this study, we evaluated the impact of HIV and meth on astrocyte senescence using in vitro and several animal models...
June 13, 2017: Aging Cell
https://www.readbyqxmd.com/read/28600811/inducible-knockdown-of-pregnancy-associated-plasma-protein-a-gene-expression-in-adult-female-mice-extends-life-span
#7
Laurie K Bale, Sally A West, Cheryl A Conover
Pregnancy-associated plasma protein-A (PAPP-A) knockout (KO) mice, generated through homologous recombination in embryonic stem cells, have a significantly increased lifespan compared to wild-type littermates. However, it is unknown whether this longevity advantage would pertain to PAPP-A gene deletion in adult animals. In the present study, we used tamoxifen (Tam)-inducible Cre recombinase-mediated excision of the floxed PAPP-A (fPAPP-A) gene in mice at 5 months of age. fPAPP-A mice, which were either positive (pos) or negative (neg) for Tam-Cre, received Tam treatment with quarterly boosters...
June 9, 2017: Aging Cell
https://www.readbyqxmd.com/read/28597569/cross-sectional-relations-of-whole-blood-mirna-expression-levels-and-hand-grip-strength-in-a-community-sample
#8
Joanne M Murabito, Jian Rong, Kathryn L Lunetta, Tianxiao Huan, Honghuang Lin, Qiang Zhao, Jane E Freedman, Kahraman Tanriverdi, Daniel Levy, Martin G Larson
MicroRNAs (miRNAs) regulate gene expression with emerging data suggesting miRNAs play a role in skeletal muscle biology. We sought to examine the association of miRNAs with grip strength in a community-based sample. Framingham Heart Study Offspring and Generation 3 participants (n = 5668 54% women, mean age 55 years, range 24, 90 years) underwent grip strength measurement and miRNA profiling using whole blood from fasting morning samples. Linear mixed-effects regression modeling of grip strength (kg) versus continuous miRNA 'Cq' values and versus binary miRNA expression was performed...
June 8, 2017: Aging Cell
https://www.readbyqxmd.com/read/28597562/reprogramming-progeria-fibroblasts-re-establishes-a-normal-epigenetic-landscape
#9
Zhaoyi Chen, Wing Y Chang, Alton Etheridge, Hilmar Strickfaden, Zhigang Jin, Gareth Palidwor, Ji-Hoon Cho, Kai Wang, Sarah Y Kwon, Carole Doré, Angela Raymond, Akitsu Hotta, James Ellis, Rita A Kandel, F Jeffrey Dilworth, Theodore J Perkins, Michael J Hendzel, David J Galas, William L Stanford
Ideally, disease modeling using patient-derived induced pluripotent stem cells (iPSCs) enables analysis of disease initiation and progression. This requires any pathological features of the patient cells used for reprogramming to be eliminated during iPSC generation. Hutchinson-Gilford progeria syndrome (HGPS) is a segmental premature aging disorder caused by the accumulation of the truncated form of Lamin A known as Progerin within the nuclear lamina. Cellular hallmarks of HGPS include nuclear blebbing, loss of peripheral heterochromatin, defective epigenetic inheritance, altered gene expression, and senescence...
June 8, 2017: Aging Cell
https://www.readbyqxmd.com/read/28585366/advances-in-therapeutic-approaches-to-extend-healthspan-a-perspective-from-the-2-nd-scripps-symposium-on-the-biology-of-aging
#10
Paul D Robbins, Laura J Niedernhofer
The 2(nd) Scripps Florida Symposium on The Biology of Aging entitled 'Advances in Therapeutic Approaches to Extend Healthspan' was held on January 22(nd) -25(th) , 2017 at The Scripps Research Institute in Jupiter, Florida. The meeting highlighted a variety of therapeutic approaches in animal models of aging that either are or soon will be in clinic trials. For example, drugs targeting senescent cells, metformin, rapalogs, NAD precursors, young plasma, mitochondrial-targeted free radical scavengers, stem cells, and stem cell factors all have shown significant preclinical efficacy...
June 6, 2017: Aging Cell
https://www.readbyqxmd.com/read/28585250/deletion-of-ghrelin-prevents-aging-associated-obesity-and-muscle-dysfunction-without-affecting-longevity
#11
Bobby Guillory, Ji-An Chen, Shivam Patel, Jiaohua Luo, Andres Splenser, Avni Mody, Michael Ding, Shiva Baghaie, Barbara Anderson, Blaga Iankova, Tripti Halder, Yamileth Hernandez, Jose M Garcia
During aging, decreases in energy expenditure and locomotor activity lead to body weight and fat gain. Aging is also associated with decreases in muscle strength and endurance leading to functional decline. Here, we show that lifelong deletion of ghrelin prevents development of obesity associated with aging by modulating food intake and energy expenditure. Ghrelin deletion also attenuated the decrease in phosphorylated adenosine monophosphate-activated protein kinase (pAMPK) and downstream mediators in muscle, and increased the number of type IIa (fatigue resistant, oxidative) muscle fibers, preventing the decline in muscle strength and endurance seen with aging...
June 6, 2017: Aging Cell
https://www.readbyqxmd.com/read/28568901/the-replicative-lifespan-extending-deletion-of-sgf73-results-in-altered-ribosomal-gene-expression-in-yeast
#12
Amanda G Mason, Renee M Garza, Mark A McCormick, Bhumil Patel, Brian K Kennedy, Lorraine Pillus, Albert R La Spada
Sgf73, a core component of SAGA, is the yeast orthologue of ataxin-7, which undergoes CAG-polyglutamine repeat expansion leading to the human neurodegenerative disease spinocerebellar ataxia type 7 (SCA7). Deletion of SGF73 dramatically extends replicative lifespan (RLS) in yeast. To further define the basis for Sgf73-mediated RLS extension, we performed ChIP-Seq, identified 388 unique genomic regions occupied by Sgf73, and noted enrichment in promoters of ribosomal protein (RP)-encoding genes. Of 388 Sgf73 binding sites, 33 correspond to 5' regions of genes implicated in RLS extension, including 20 genes encoding RPs...
May 31, 2017: Aging Cell
https://www.readbyqxmd.com/read/28560849/transcription-factors-cep-1-p53-and-ceh-23-collaborate-with-aak-2-ampk-to-modulate-longevity-in-caenorhabditis-elegans
#13
Hsin-Wen Chang, Steve Pisano, Amaresh Chaturbedi, Jennifer Chen, Sarah Gordon, Aiswarya Baruah, Siu Sylvia Lee
A decline in mitochondrial electron transport chain (ETC) function has long been implicated in aging and various diseases. Recently, moderate mitochondrial ETC dysfunction has been found to prolong lifespan in diverse organisms, suggesting a conserved and complex role of mitochondria in longevity determination. Several nuclear transcription factors have been demonstrated to mediate the lifespan extension effect associated with partial impairment of the ETC, suggesting that compensatory transcriptional response to be crucial...
May 30, 2017: Aging Cell
https://www.readbyqxmd.com/read/28556540/sustained-nf%C3%AE%C2%BAb-inhibition-improves-insulin-sensitivity-but-is-detrimental-to-muscle-health
#14
Ning Zhang, Joseph M Valentine, You Zhou, Mengyao E Li, Yiqiang Zhang, Arunabh Bhattacharya, Michael E Walsh, Katherine E Fischer, Steven N Austad, Pawel Osmulski, Maria Gaczynska, Steven E Shoelson, Holly Van Remmen, Hung I Chen, Yidong Chen, Hanyu Liang, Nicolas Musi
Older adults universally suffer from sarcopenia and approximately 60-70% are diabetic or prediabetic. Nonetheless, the mechanisms underlying these aging-related metabolic disorders are unknown. NFκB has been implicated in the pathogenesis of several aging-related pathologies including sarcopenia and type 2 diabetes and has been proposed as a target against them. NFκB also is thought to mediate muscle wasting seen with disuse, denervation, and some systemic diseases (e.g., cancer, sepsis). We tested the hypothesis that lifelong inhibition of the classical NFκB pathway would protect against aging-related sarcopenia and insulin resistance...
May 29, 2017: Aging Cell
https://www.readbyqxmd.com/read/28556428/identification-of-tissue-specific-transcriptional-markers-of-caloric-restriction-in-the-mouse-and-their-use-to-evaluate-caloric-restriction-mimetics
#15
Jamie L Barger, James M Vann, Nicole L Cray, Thomas D Pugh, Angela Mastaloudis, Shelly N Hester, Steven M Wood, Michael A Newton, Richard Weindruch, Tomas A Prolla
Caloric restriction (CR) without malnutrition has been shown to retard several aspects of the aging process and to extend lifespan in different species. There is strong interest in the identification of CR mimetics (CRMs), compounds that mimic the beneficial effects of CR on lifespan and healthspan without restriction of energy intake. Identification of CRMs in mammals is currently inefficient due to the lack of screening tools. We have performed whole-genome transcriptional profiling of CR in seven mouse strains (C3H/HeJ, CBA/J, DBA/2J, B6C3F1/J, 129S1/SvImJ, C57BL/6J, and BALB/cJ) in white adipose tissue (WAT), gastrocnemius muscle, heart, and brain neocortex...
May 26, 2017: Aging Cell
https://www.readbyqxmd.com/read/28544111/kallistatin-reduces-vascular-senescence-and-aging-by-regulating-microrna-34a-sirt1-pathway
#16
Youming Guo, Pengfei Li, Lin Gao, Jingmei Zhang, Zhirong Yang, Grant Bledsoe, Eugene Chang, Lee Chao, Julie Chao
Kallistatin, an endogenous protein, protects against vascular injury by inhibiting oxidative stress and inflammation in hypertensive rats and enhancing the mobility and function of endothelial progenitor cells (EPCs). We aimed to determine the role and mechanism of kallistatin in vascular senescence and aging using cultured EPCs, streptozotocin (STZ)-induced diabetic mice, and Caenorhabditis elegans (C. elegans). Human kallistatin significantly decreased TNF-α-induced cellular senescence in EPCs, as indicated by reduced senescence-associated β-galactosidase activity and plasminogen activator inhibitor-1 expression, and elevated telomerase activity...
May 24, 2017: Aging Cell
https://www.readbyqxmd.com/read/28544616/biochemical-isolation-of-myonuclei-employed-to-define-changes-to-the-myonuclear-proteome-that-occur-with-aging
#17
Alicia A Cutler, Eric B Dammer, Duc M Doung, Nicholas T Seyfried, Anita H Corbett, Grace K Pavlath
Skeletal muscle aging is accompanied by loss of muscle mass and strength. Examining changes in myonuclear proteins with age would provide insight into molecular processes which regulate these profound changes in muscle physiology. However, muscle tissue is highly adapted for contraction and thus comprised largely of contractile proteins making the nuclear proteins difficult to identify from whole muscle samples. By developing a method to purify myonuclei from whole skeletal muscle, we were able to collect myonuclei for analysis by flow cytometry, biochemistry, and mass spectrometry...
May 23, 2017: Aging Cell
https://www.readbyqxmd.com/read/28544158/molecular-and-physiological-manifestations-and-measurement-of-aging-in-humans
#18
REVIEW
Sadiya S Khan, Benjamin D Singer, Douglas E Vaughan
Biological aging is associated with a reduction in the reparative and regenerative potential in tissues and organs. This reduction manifests as a decreased physiological reserve in response to stress (termed homeostenosis) and a time-dependent failure of complex molecular mechanisms that cumulatively create disorder. Aging inevitably occurs with time in all organisms and emerges on a molecular, cellular, organ, and organismal level with genetic, epigenetic, and environmental modulators. Individuals with the same chronological age exhibit differential trajectories of age-related decline, and it follows that we should assess biological age distinctly from chronological age...
May 23, 2017: Aging Cell
https://www.readbyqxmd.com/read/28544360/impairment-of-insulin-signalling-in-peripheral-tissue-fails-to-extend-murine-lifespan
#19
Troy L Merry, Doreen Kuhlow, Beate Laube, Doris Pöhlmann, Andreas F H Pfeiffer, C Ronald Kahn, Michael Ristow, Kim Zarse
Impaired insulin/IGF1 signalling has been shown to extend lifespan in model organisms ranging from yeast to mammals. Here we sought to determine the effect of targeted disruption of the insulin receptor (IR) in non-neuronal tissues of adult mice on the lifespan. We induced hemizygous (PerIRKO(+/-) ) or homozygous (PerIRKO(-/-) ) disruption of the IR in peripheral tissue of 15-weeks-old mice using a tamoxifen-inducible Cre transgenic mouse with only peripheral tissue expression, and subsequently monitored glucose metabolism, insulin signalling and spontaneous death rates over 4 years...
May 22, 2017: Aging Cell
https://www.readbyqxmd.com/read/28544226/short-term-rapamycin-treatment-increases-ovarian-lifespan-in%C3%A2-young-and-middle-aged-female-mice
#20
Xiaowei Dou, Yan Sun, Jiazhao Li, Jing Zhang, Dandan Hao, Wenwen Liu, Rui Wu, Feifei Kong, Xiaoxu Peng, Jing Li
Although age-related ovarian failure in female mammals cannot be reversed, recent strategies have focused on improving reproductive capacity with age, and rapamycin is one such intervention that has shown a potential for preserving the ovarian follicle pool and preventing premature ovarian failure. However, the application is limited because of its detrimental effects on follicular development and ovulation during long-term treatment. Herein, we shortened the rapamycin administration to 2 weeks and applied the protocol to both young (8 weeks) and middle-aged (8 months) mouse models...
May 22, 2017: Aging Cell
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