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Aging Cell

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https://www.readbyqxmd.com/read/28229533/expansion-of-myeloid-derived-suppressor-cells-with-aging-in-the-bone-marrow-of-mice-through-a-nf-%C3%AE%C2%BAb-dependent-mechanism
#1
Rafael R Flores, Cheryl L Clauson, Joonseok Cho, Byeong-Chel Lee, Sara J McGowan, Darren J Baker, Laura J Niedernhofer, Paul D Robbins
With aging, there is progressive loss of tissue homeostasis and functional reserve, leading to an impaired response to stress and an increased risk of morbidity and mortality. A key mediator of the cellular response to damage and stress is the transcription factor NF-κB. We demonstrated previously that NF-κB transcriptional activity is upregulated in tissues from both natural aged mice and in a mouse model of a human progeroid syndrome caused by defective repair of DNA damage (ERCC1-deficient mice). We also demonstrated that genetic reduction in the level of the NF-κB subunit p65(RelA) in the Ercc1(-/∆) progeroid mouse model of accelerated aging delayed the onset of age-related pathology including muscle wasting, osteoporosis, and intervertebral disk degeneration...
February 23, 2017: Aging Cell
https://www.readbyqxmd.com/read/28185435/evidence-that-a-mitochondrial-death-spiral-underlies-antagonistic-pleiotropy
#2
REVIEW
Michael Stern
The antagonistic pleiotropy (AP) theory posits that aging occurs because alleles that are detrimental in older organisms are beneficial to growth early in life and thus are maintained in populations. Although genes of the insulin signaling pathway likely participate in AP, the insulin-regulated cellular correlates of AP have not been identified. The mitochondrial quality control process called mitochondrial autophagy (mitophagy), which is inhibited by insulin signaling, might represent a cellular correlate of AP...
February 9, 2017: Aging Cell
https://www.readbyqxmd.com/read/28185406/detecting-senescence-a-new-method-for-an-old-pigment
#3
Hanna Salmonowicz, João F Passos
Cellular senescence is a state of irreversible cell cycle arrest induced by different types of cellular stresses. The field of senescence has made significant advances in the understanding of many of the mechanisms governing this phenomenon; however, a universal biomarker that unambiguously distinguishes senescent from proliferating cells has not been found. In this issue of Aging Cell, Evangelou and colleagues developed a sensitive method for identification of senescent cells in different types of biological material based on the detection of lipofuscin using an analogue of Sudan Black B (SBB) histochemical dye coupled with biotin, which they named GL13...
February 9, 2017: Aging Cell
https://www.readbyqxmd.com/read/28181388/muscle-strength-mediates-the-relationship-between-mitochondrial-energetics-and-walking-performance
#4
Ariel C Zane, David A Reiter, Michelle Shardell, Donnie Cameron, Eleanor M Simonsick, Kenneth W Fishbein, Stephanie A Studenski, Richard G Spencer, Luigi Ferrucci
Skeletal muscle mitochondrial oxidative capacity declines with age and negatively affects walking performance, but the mechanism for this association is not fully clear. We tested the hypothesis that impaired oxidative capacity affects muscle performance and, through this mechanism, has a negative effect on walking speed. Muscle mitochondrial oxidative capacity was measured by in vivo phosphorus magnetic resonance spectroscopy as the postexercise phosphocreatine resynthesis rate, kPCr , in 326 participants (154 men), aged 24-97 years (mean 71), in the Baltimore Longitudinal Study of Aging...
February 9, 2017: Aging Cell
https://www.readbyqxmd.com/read/28160413/accelerated-aging-exacerbates-a-pre-existing-pathology-in-a-tau-transgenic-mouse-model
#5
Liviu-Gabriel Bodea, Harrison Tudor Evans, Ann Van der Jeugd, Lars M Ittner, Fabien Delerue, Jillian Kril, Glenda Halliday, John Hodges, Mathew C Kiernan, Jürgen Götz
Age is a critical factor in the prevalence of tauopathies, including Alzheimer's disease. To observe how an aging phenotype interacts with and affects the pathological intracellular accumulation of hyperphosphorylated tau, the tauopathy mouse model pR5 (expressing P301L mutant human tau) was back-crossed more than ten times onto a senescence-accelerated SAMP8 background to establish the new strain, SApT. Unlike SAMP8 mice, pR5 mice are characterized by a robust tau pathology particularly in the amygdala and hippocampus...
February 4, 2017: Aging Cell
https://www.readbyqxmd.com/read/28156058/aging-and-caloric-restriction-impact-adipose-tissue-adiponectin-and-circulating-lipids
#6
Karl N Miller, Maggie S Burhans, Josef P Clark, Porsha R Howell, Michael A Polewski, Tyler M DeMuth, Kevin W Eliceiri, Mary J Lindstrom, James M Ntambi, Rozalyn M Anderson
Adipose tissue expansion has been associated with system-wide metabolic dysfunction and increased vulnerability to diabetes, cancer, and cardiovascular disease. A reduction in adiposity is a hallmark of caloric restriction (CR), an intervention that extends longevity and delays the onset of these same age-related conditions. Despite these parallels, the role of adipose tissue in coordinating the metabolism of aging is poorly defined. Here, we show that adipose tissue metabolism and secretory profiles change with age and are responsive to CR...
February 3, 2017: Aging Cell
https://www.readbyqxmd.com/read/28156052/melatonin-alleviates-lipopolysaccharide-compromised-integrity-of-blood-brain-barrier-through-activating-amp-activated-protein-kinase-in-old-mice
#7
Xiaona Wang, Gai-Xiu Xue, Wen-Cao Liu, Hui Shu, Mengwei Wang, Yanyun Sun, Xiaojing Liu, Yi Eve Sun, Chun-Feng Liu, Jie Liu, Wenlan Liu, Xinchun Jin
Blood-brain barrier (BBB) dysfunction is considered to be an early event in the pathogenesis of a variety of neurological diseases in old patients, and this could occur in old people even when facing common stress. However, the mechanism remains to be defined. In this study, we tested the hypothesis that decreased melatonin levels may account for the BBB disruption in old mice challenged with lipopolysaccharide (LPS), which mimicked the common stress of sepsis. Mice (24-28 months of age) received melatonin (10 mg kg(-1)  day(-1) , intraperitoneally, i...
February 3, 2017: Aging Cell
https://www.readbyqxmd.com/read/28139067/the-effects-of-graded-levels-of-calorie-restriction-ix-global-metabolomic-screen-reveals-modulation-of-carnitines-sphingolipids-and-bile-acids-in-the-liver-of-c57bl-6-mice
#8
Cara L Green, Sharon E Mitchell, Davina Derous, Yingchun Wang, Luonan Chen, Jing-Dong J Han, Daniel E L Promislow, David Lusseau, Alex Douglas, John R Speakman
Calorie restriction (CR) remains the most robust intervention to extend lifespan and improve health span. Using a global mass spectrometry-based metabolomic approach, we identified 193 metabolites that were significantly differentially expressed (SDE) in the livers of C57BL/6 mice, fed graded levels of CR (10, 20, 30 and 40% CR) compared to mice fed ad libitum for 12 h a day. The differential expression of metabolites also varied with the different feeding groups. Pathway analysis revealed that graded CR had an impact on carnitine synthesis and the carnitine shuttle pathway, sphingosine-1-phosphate (S1P) signalling and methionine metabolism...
January 31, 2017: Aging Cell
https://www.readbyqxmd.com/read/28127848/mir-30c-protects-diabetic-nephropathy-by-suppressing-epithelial-to-mesenchymal-transition-in-db-db-mice
#9
Yanru Zhao, Zhongwei Yin, Huaping Li, Jiahui Fan, Shenglan Yang, Chen Chen, Dao Wen Wang
Epithelial-to-mesenchymal transition (EMT) plays a significant role in tubulointerstitial fibrosis, which is a hallmark of diabetic nephropathy. Thus, identifying the mechanisms of EMT activation could be meaningful. In this study, loss of miR-30c accompanied with increased EMT was observed in renal tubules of db/db mice and cultured HK2 cells exposed to high glucose. To further explore the roles of miR-30c in EMT and tubulointerstitial fibrosis, recombinant adeno-associated viral vector was applied to manipulate the expression of miR-30c...
January 27, 2017: Aging Cell
https://www.readbyqxmd.com/read/28124509/a-novel-single-cell-method-provides-direct-evidence-of-persistent-dna-damage-in-senescent-cells-and-aged-mammalian-tissues
#10
Alessandro Galbiati, Christian Beauséjour, Fabrizio d'Adda di Fagagna
The DNA damage response (DDR) arrests cell cycle progression until DNA lesions, like DNA double-strand breaks (DSBs), are repaired. The presence of DSBs in cells is usually detected by indirect techniques that rely on the accumulation of proteins at DSBs, as part of the DDR. Such detection may be biased, as some factors and their modifications may not reflect physical DNA damage. The dependency on DDR markers of DSB detection tools has left questions unanswered. In particular, it is known that senescent cells display persistent DDR foci, that we and others have proposed to be persistent DSBs, resistant to endogenous DNA repair activities...
January 26, 2017: Aging Cell
https://www.readbyqxmd.com/read/28124466/cellular-senescence-in-osteoarthritis-pathology
#11
REVIEW
Kendal McCulloch, Gary J Litherland, Taranjit Singh Rai
Cellular senescence is a state of stable proliferation arrest of cells. The senescence pathway has many beneficial effects and is seen to be activated in damaged/stressed cells, as well as during embryonic development and wound healing. However, the persistence and accumulation of senescent cells in various tissues can also impair function and have been implicated in the pathogenesis of many age-related diseases. Osteoarthritis (OA), a severely debilitating chronic condition characterized by progressive tissue remodeling and loss of joint function, is the most prevalent disease of the synovial joints, and increasing age is the primary OA risk factor...
January 26, 2017: Aging Cell
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
#12
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
#13
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
#14
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
#15
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
#16
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
#17
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
#18
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
#19
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
#20
José Renato Pinto, Judy Muller-Delp, P Bryant Chase
No abstract text is available yet for this article.
December 23, 2016: Aging Cell
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