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Aging Cell

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https://read.qxmd.com/read/30773786/the-angiotensin-1-7-mas-receptor-axis-protects-from-endothelial-cell-senescence-via-klotho-and-nrf2-activation
#1
Alejandra Romero, Álvaro San Hipólito-Luengo, Laura A Villalobos, Susana Vallejo, Inés Valencia, Patrycja Michalska, Natalia Pajuelo-Lozano, Isabel Sánchez-Pérez, Rafael León, José Luis Bartha, María Jesús Sanz, Jorge D Erusalimsky, Carlos F Sánchez-Ferrer, Tania Romacho, Concepción Peiró
Endothelial cell senescence is a hallmark of vascular aging that predisposes to vascular disease. We aimed to explore the capacity of the renin-angiotensin system (RAS) heptapeptide angiotensin (Ang)-(1-7) to counteract human endothelial cell senescence and to identify intracellular pathways mediating its potential protective action. In human umbilical vein endothelial cell (HUVEC) cultures, Ang II promoted cell senescence, as revealed by the enhancement in senescence-associated galactosidase (SA-β-gal+) positive staining, total and telomeric DNA damage, adhesion molecule expression, and human mononuclear adhesion to HUVEC monolayers...
February 17, 2019: Aging Cell
https://read.qxmd.com/read/30773784/elimination-of-senescent-osteoclast-progenitors-has-no-effect-on-the-age-associated-loss-of-bone-mass-in-mice
#2
Ha-Neui Kim, Jianhui Chang, Srividhya Iyer, Li Han, Judith Campisi, Stavros C Manolagas, Daohong Zhou, Maria Almeida
Both an increase in osteoclast and a decrease in osteoblast numbers contribute to skeletal aging. Markers of cellular senescence, including expression of the cyclin inhibitor p16, increase with aging in several bone cell populations. The elimination of p16-expressing cells in old mice, using the INK-ATTAC transgene, increases bone mass indicating that senescent cells contribute to skeletal aging. However, the identity of the senescent cells and the extent to which ablation of p16-expressing cells may prevent skeletal aging remain unknown...
February 17, 2019: Aging Cell
https://read.qxmd.com/read/30773782/daf-16-stabilizes-the-aging-transcriptome-and-is-activated-in-mid-aged-caenorhabditis-elegans-to-cope-with-internal-stress
#3
Shang-Tong Li, Han-Qing Zhao, Pan Zhang, Chung-Yi Liang, Yan-Ping Zhang, Ao-Lin Hsu, Meng-Qiu Dong
The roles and regulatory mechanisms of transcriptome changes during aging are unclear. It has been proposed that the transcriptome suffers decay during aging owing to age-associated down-regulation of transcription factors. In this study, we characterized the role of a transcription factor DAF-16, which is a highly conserved lifespan regulator, in the normal aging process of Caenorhabditis elegans. We found that DAF-16 translocates into the nucleus in aged wild-type worms and activates the expression of hundreds of genes in response to age-associated cellular stress...
February 17, 2019: Aging Cell
https://read.qxmd.com/read/30773781/kin-4-mast-kinase-promotes-pten-mediated-longevity-of-caenorhabditis-elegans-via-binding-through-a-pdz-domain
#4
Seon Woo A An, Eun-Seok Choi, Wooseon Hwang, Heehwa G Son, Jae-Seong Yang, Keunhee Seo, Hyun-Jun Nam, Nhung T H Nguyen, Eun Ji E Kim, Bo Kyoung Suh, Youngran Kim, Shunji Nakano, Youngjae Ryu, Chang Man Ha, Ikue Mori, Sang Ki Park, Joo-Yeon Yoo, Sanguk Kim, Seung-Jae V Lee
PDZ domain-containing proteins (PDZ proteins) act as scaffolds for protein-protein interactions and are crucial for a variety of signal transduction processes. However, the role of PDZ proteins in organismal lifespan and aging remains poorly understood. Here, we demonstrate that KIN-4, a PDZ domain-containing microtubule-associated serine-threonine (MAST) protein kinase, is a key longevity factor acting through binding PTEN phosphatase in Caenorhabditis elegans. Through a targeted genetic screen for PDZ proteins, we find that kin-4 is required for the long lifespan of daf-2/insulin/IGF-1 receptor mutants...
February 17, 2019: Aging Cell
https://read.qxmd.com/read/30768754/accelerated-bio-cognitive-aging-in-down-syndrome-state-of-the-art-and-possible-deceleration-strategies
#5
REVIEW
Claudio Franceschi, Paolo Garagnani, Noémie Gensous, Maria Giulia Bacalini, Maria Conte, Stefano Salvioli
Down syndrome (DS) has been proposed by George Martin as a segmental progeroid syndrome since 1978. In fact, DS persons suffer from several age-associated disorders much earlier than euploid persons. Furthermore, a series of recent studies have found that DS persons display elevated levels of age biomarkers, thus supporting the notion that DS is a progeroid trait. Nowadays, due to the progressive advancements in social inclusion processes and medical assistance, DS persons live much longer than in the past; therefore, the early-onset health problems of these persons are becoming an urgent and largely unmet social and medical burden...
February 15, 2019: Aging Cell
https://read.qxmd.com/read/30768748/the-exceptional-longevity-of-the-naked-mole-rat-may-be-explained-by-mitochondrial-antioxidant-defenses
#6
Daniel Munro, Cécile Baldy, Matthew E Pamenter, Jason R Treberg
Naked mole-rats (NMRs) are mouse-sized mammals that exhibit an exceptionally long lifespan (>30 vs. <4 years for mice), and resist aging-related pathologies such as cardiovascular and pulmonary diseases, cancer, and neurodegeneration. However, the mechanisms underlying this exceptional longevity and disease resistance remain poorly understood. The oxidative stress theory of aging posits that (a) senescence results from the accumulation of oxidative damage inflicted by reactive oxygen species (ROS) of mitochondrial origin, and (b) mitochondria of long-lived species produce less ROS than do mitochondria of short-lived species...
February 15, 2019: Aging Cell
https://read.qxmd.com/read/30767411/dynamin-like-protein-1-cleavage-by-calpain-in-alzheimer-s-disease
#7
Sirui Jiang, Changjuan Shao, Fangqiang Tang, Wenzhang Wang, Xiongwei Zhu
Abnormal mitochondrial dynamics contributes to mitochondrial dysfunction in Alzheimer's disease (AD), yet the underlying mechanism remains elusive. In the current study, we reported that DLP1, the key mitochondrial fission GTPase, is a substrate of calpain which produced specific N-terminal DLP1 cleavage fragments. In addition, various AD-related insults such as exposure to glutamate, soluble amyloid-β oligomers, or reagents inducing tau hyperphosphorylation (i.e., okadaic acid) led to calpain-dependent cleavage of DLP1 in primary cortical neurons...
February 14, 2019: Aging Cell
https://read.qxmd.com/read/30746836/conservation-of-physiological-dysregulation-signatures-of-aging-across-primates
#8
Gabriel Dansereau, Tina W Wey, Véronique Legault, Marie A Brunet, Joseph W Kemnitz, Luigi Ferrucci, Alan A Cohen
Two major goals in the current biology of aging are to identify general mechanisms underlying the aging process and to explain species differences in aging. Recent research in humans suggests that one important driver of aging is dysregulation, the progressive loss of homeostasis in complex biological networks. Yet, there is a lack of comparative data for this hypothesis, and we do not know whether dysregulation is widely associated with aging or how well signals of homeostasis are conserved. To address this knowledge gap, we use unusually detailed longitudinal biomarker data from 10 species of nonhuman primates housed in research centers and data from two human populations to test the hypotheses that (a) greater dysregulation is associated with aging across primates and (b) physiological states characterizing homeostasis are conserved across primates to degrees associated with phylogenetic proximity...
February 11, 2019: Aging Cell
https://read.qxmd.com/read/30746828/hyperoxygenation-revitalizes-alzheimer-s-disease-pathology-through-the-upregulation-of-neurotrophic-factors
#9
Juli Choi, Hye-Jin Kwon, Jung-Eun Lee, Yunjin Lee, Ju-Young Seoh, Pyung-Lim Han
Alzheimer's disease (AD) is a neurodegenerative disease characterized by Aβ-induced pathology and progressive cognitive decline. The incidence of AD is growing globally, yet a prompt and effective remedy is not available. Aging is the greatest risk factor for AD. Brain aging proceeds with reduced vascularization, which can cause low oxygen (O2 ) availability. Accordingly, the question may be raised whether O2 availability in the brain affects AD pathology. We found that Tg-APP/PS1 mice treated with 100% O2 at increased atmospheric pressure in a chamber exhibited markedly reduced Aβ accumulation and hippocampal neuritic atrophy, increased hippocampal neurogenesis, and profoundly improved the cognitive deficits on the multiple behavioral test paradigms...
February 11, 2019: Aging Cell
https://read.qxmd.com/read/30740872/17-%C3%AE-estradiol-ameliorates-age-associated-sarcopenia-and-improves-late-life-physical-function-in-male-mice-but-not-in-females-or-castrated-males
#10
Michael Garratt, Danielle Leander, Kaitlyn Pifer, Brian Bower, Jonathan J Herrera, Sharlene M Day, Oliver Fiehn, Susan V Brooks, Richard A Miller
Pharmacological treatments can extend mouse lifespan, but lifespan effects often differ between sexes. 17-α estradiol (17aE2), a less feminizing structural isomer of 17-β estradiol, produces lifespan extension only in male mice, suggesting a sexually dimorphic mechanism of lifespan regulation. We tested whether these anti-aging effects extend to anatomical and functional aging-important in late-life health-and whether gonadally derived hormones control aging responses to 17aE2 in either sex. While 17aE2 started at 4 months of age diminishes body weight in both sexes during adulthood, in late-life 17aE2-treated mice better maintain body weight...
February 10, 2019: Aging Cell
https://read.qxmd.com/read/30734981/age-dependent-changes-and-biomarkers-of-aging-in-caenorhabditis-elegans
#11
REVIEW
Heehwa G Son, Ozlem Altintas, Eun Ji E Kim, Sujeong Kwon, Seung-Jae V Lee
Caenorhabditis elegans is an exceptionally valuable model for aging research because of many advantages, including its genetic tractability, short lifespan, and clear age-dependent physiological changes. Aged C. elegans display a decline in their anatomical and functional features, including tissue integrity, motility, learning and memory, and immunity. Caenorhabditis elegans also exhibit many age-associated changes in the expression of microRNAs and stress-responsive genes and in RNA and protein quality control systems...
February 8, 2019: Aging Cell
https://read.qxmd.com/read/30719830/low-plasma-lysophosphatidylcholines-are-associated-with-impaired-mitochondrial-oxidative-capacity-in-adults-in-the-baltimore-longitudinal-study-of-aging
#12
Richard D Semba, Pingbo Zhang, Fatemeh Adelnia, Kai Sun, Marta Gonzalez-Freire, Norman Salem, Nicholas Brennan, Richard G Spencer, Kenneth Fishbein, Mohammed Khadeer, Michelle Shardell, Ruin Moaddel, Luigi Ferrucci
The decrease in skeletal muscle mitochondrial oxidative capacity with age adversely affects muscle strength and physical performance. Factors that are associated with this decrease have not been well characterized. Low plasma lysophosphatidylcholines (LPC), a major class of systemic bioactive lipids, are predictive of aging phenotypes such as cognitive impairment and decline of gait speed in older adults. Therefore, we tested the hypothesis that low plasma LPC are associated with impaired skeletal muscle mitochondrial oxidative capacity...
February 4, 2019: Aging Cell
https://read.qxmd.com/read/30712319/epigenetic-age-is-a-cell-intrinsic-property-in-transplanted-human-hematopoietic-cells
#13
Arne Søraas, Mieko Matsuyama, Marcos de Lima, David Wald, Jochen Buechner, Tobias Gedde-Dahl, Camilla Lund Søraas, Brian Chen, Luigi Ferrucci, John Arne Dahl, Steve Horvath, Shigemi Matsuyama
The age of tissues and cells can be accurately estimated by DNA methylation analysis. The multitissue DNA methylation (DNAm) age predictor combines the DNAm levels of 353 CpG dinucleotides to arrive at an age estimate referred to as DNAm age. Recent studies based on short-term observations showed that the DNAm age of reconstituted blood following allogeneic hematopoietic stem cell transplantation (HSCT) reflects the age of the donor. However, it is not known whether the DNAm age of donor blood remains independent of the recipient's age over the long term...
February 2, 2019: Aging Cell
https://read.qxmd.com/read/30710410/identification-of-stable-senescence-associated-reference-genes
#14
Alejandra Hernandez-Segura, Richard Rubingh, Marco Demaria
Cellular senescence is a state of permanent cell cycle arrest activated in response to damaging stimuli. Many hallmarks associated with senescent cells are measured by quantitative real-time PCR (qPCR). As the selection of stable reference genes for interpretation of qPCR data is often overlooked, we performed a systematic review to understand normalization strategies entailed in experiments involving senescent cells. We found that, in violation of the Minimum Information for publication of qPCR Experiments (MIQE) guidelines, most reports used only one reference gene to normalize qPCR data, and that stability of the reference genes was either not tested or not reported...
February 1, 2019: Aging Cell
https://read.qxmd.com/read/30706990/activation-of-mt2-receptor-ameliorates-dendritic-abnormalities-in-alzheimer-s-disease-via-c-ebp%C3%AE-mir-125b-pathway
#15
Hui Tang, Mei Ma, Ying Wu, Man-Fei Deng, Fan Hu, Hasan A M M Almansoub, He-Zhou Huang, Ding-Qi Wang, Lan-Ting Zhou, Na Wei, Hengye Man, Youming Lu, Dan Liu, Ling-Qiang Zhu
Impairments of dendritic trees and spines have been found in many neurodegenerative diseases, including Alzheimer's disease (AD), in which the deficits of melatonin signal pathway were reported. Melatonin receptor 2 (MT2) is widely expressed in the hippocampus and mediates the biological functions of melatonin. It is known that melatonin application is protective to dendritic abnormalities in AD. However, whether MT2 is involved in the neuroprotection and the underlying mechanisms are not clear. Here, we first found that MT2 is dramatically reduced in the dendritic compartment upon the insult of oligomer Aβ...
February 1, 2019: Aging Cell
https://read.qxmd.com/read/30706629/hif1%C3%AE-mediated-aimp3-suppression-delays-stem-cell-aging-via-the-induction-of-autophagy
#16
Chul Kim, Ji-Min Park, Youngsook Song, Sunghoon Kim, Jisook Moon
Senescence in stem cells, which occurs as a consequence of chronic responses to the environment, defines the capacity of stem cells for proliferation and differentiation as well as their potential for tissue regeneration and homeostasis maintenance. Although stem cells reside under low oxygen pressure and the availability of oxygen is known to be a crucial determinant in their fate, the key modulators in stem cell aging and the underlying mechanism have yet to be unraveled. Human placenta-derived mesenchymal stem cells (hpMSCs) were cultured under hypoxia (3% O2 ) or normoxia (21% O2 ) to investigate the key factors that regulate stem cell senescence under hypoxic conditions...
January 31, 2019: Aging Cell
https://read.qxmd.com/read/30706626/extranuclear-dna-accumulates-in-aged-cells-and-contributes-to-senescence-and-inflammation
#17
Yuk Yuen Lan, James M Heather, Thomas Eisenhaure, Christopher Stuart Garris, David Lieb, Raktima Raychowdhury, Nir Hacohen
Systemic inflammation is central to aging-related conditions. However, the intrinsic factors that induce inflammation are not well understood. We previously identified a cell-autonomous pathway through which damaged nuclear DNA is trafficked to the cytosol where it activates innate cytosolic DNA sensors that trigger inflammation. These results led us to hypothesize that DNA released after cumulative damage contributes to persistent inflammation in aging cells through a similar mechanism. Consistent with this notion, we found that older cells harbored higher levels of extranuclear DNA compared to younger cells...
January 31, 2019: Aging Cell
https://read.qxmd.com/read/30688027/acarbose-improves-health-and-lifespan-in-aging-het3-mice
#18
David E Harrison, Randy Strong, Silvestre Alavez, Clinton Michael Astle, John DiGiovanni, Elizabeth Fernandez, Kevin Flurkey, Michael Garratt, Jonathan A L Gelfond, Martin A Javors, Moshe Levi, Gordon J Lithgow, Francesca Macchiarini, James F Nelson, Stacey J Sukoff Rizzo, Thomas J Slaga, Tim Stearns, John Erby Wilkinson, Richard A Miller
To follow-up on our previous report that acarbose (ACA), a drug that blocks postprandial glucose spikes, increases mouse lifespan, we studied ACA at three doses: 400, 1,000 (the original dose), and 2,500 ppm, using genetically heterogeneous mice at three sites. Each dose led to a significant change (by log-rank test) in both sexes, with larger effects in males, consistent with the original report. There were no significant differences among the three doses. The two higher doses produced 16% or 17% increases in median longevity of males, but only 4% or 5% increases in females...
January 27, 2019: Aging Cell
https://read.qxmd.com/read/30680911/long-term-intake-of-phenolic-compounds-attenuates-age-related-cardiac-remodeling
#19
Stéphanie Chacar, Joelle Hajal, Youakim Saliba, Patrick Bois, Nicolas Louka, Richard G Maroun, Jean-François Faivre, Nassim Fares
With the onset of advanced age, cardiac-associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long-term impact of phenolic compounds (PC) on age-associated cardiac remodeling. Three-month-old Wistar rats were treated for 14 months till middle-age with either 2...
January 24, 2019: Aging Cell
https://read.qxmd.com/read/30667167/the-trkb-t1-receptor-mediates-bdnf-induced-migration-of-aged-cardiac-microvascular-endothelial-cells-by-recruiting-willin
#20
Zhefeng Wang, Yilin Chen, Xuwei Chen, Xin Zheng, Ganlin Xu, Ziqiang Yuan, Hui Zhao, Wensheng Chen, Lilin Li, Nianjue Zheng, Xiaotao Shen, Yanmei Li, Xufeng Qi, Dongqing Cai
The mechanism of age-related decline in the angiogenic potential of the myocardium is not yet fully understood. Our previous report revealed that the aging of cardiac microvascular endothelial cells (CMECs) led to changes in their expression of receptor Trk isoforms: among the three isoforms (TrkB-FL, TrkB-T1 and TrkB-T2), only the truncated TrkB-T1 isoform continued to be expressed in aged CMECs, which led to decreased migration of CMECs in aging hearts. Thus far, how BDNF induces signalling through the truncated TrkB-T1 isoform in aged CMECs remains unclear...
January 22, 2019: Aging Cell
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