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Aging Cell

Audrey Griveau, Clotilde Wiel, Benjamin Le Calvé, Dorian V Ziegler, Sophia Djebali, Marine Warnier, Nadine Martin, Jacqueline Marvel, David Vindrieux, Martin O Bergo, David Bernard
Hutchinson-Gilford progeria syndrome (HGPS) is a lethal premature aging that recapitulates many normal aging characteristics. This disorder is caused by mutation in the LMNA gene leading to the production of progerin which induces misshapen nuclei, cellular senescence, and aging. We previously showed that the phospholipase A2 receptor (PLA2R1) promotes senescence induced by replicative, oxidative, and oncogenic stress but its role during progerin-induced senescence and in progeria is currently unknown. Here, we show that knockdown of PLA2R1 prevented senescence induced by progerin expression in human fibroblasts and markedly delayed senescence of HGPS patient-derived fibroblasts...
September 14, 2018: Aging Cell
Xingjie Ma, Marine Warnier, Clotilde Raynard, Mylène Ferrand, Olivier Kirsh, Pierre-Antoine Defossez, Nadine Martin, David Bernard
Calcium signaling is emerging as a key pathway controlling cellular senescence, a stable cell proliferation arrest playing a fundamental role in pathophysiological conditions, such as embryonic development, wound healing, cancer, and aging. However, how calcium signaling is regulated is still only partially understood. The inositol 1, 4, 5-trisphosphate receptor type 2 (ITPR2), an endoplasmic reticulum calcium release channel, was recently shown to critically contribute to the implementation of senescence, but how ITPR2 expression is controlled is unclear...
September 14, 2018: Aging Cell
Mehrnaz Shamalnasab, Simon-Pierre Gravel, Julie St-Pierre, Lionel Breton, Sibylle Jäger, Hugo Aguilaniu
Plant extracts containing salicylates are probably the most ancient remedies to reduce fever and ease aches of all kind. Recently, it has been shown that salicylates activate adenosine monophosphate-activated kinase (AMPK), which is now considered as a promising target to slow down aging and prevent age-related diseases in humans. Beneficial effects of AMPK activation on lifespan have been discovered in the model organism Caenorhabditis elegans (C. elegans). Indeed, salicylic acid and acetylsalicylic acid extend lifespan in worms by activating AMPK and the forkhead transcription factor DAF-16/FOXO...
September 7, 2018: Aging Cell
Hangsak Huy, Hae Young Song, Mi Jeong Kim, Won Sam Kim, Dong Oh Kim, Jae-Eun Byun, Jungwoon Lee, Young-Jun Park, Tae-Don Kim, Suk Ran Yoon, Eun-Ji Choi, Chul-Ho Lee, Ji-Yoon Noh, Haiyoung Jung, Inpyo Choi
Aging is associated with an inevitable and universal loss of cell homeostasis and restricts an organism's lifespan by an increased susceptibility to diseases and tissue degeneration. The glucose uptake associated with producing energy for cell survival is one of the major causes of ROS production under physiological conditions. However, the overall mechanisms by which glucose uptake results in cellular senescence remain mysterious. In this study, we found that TXNIP deficiency accelerated the senescent phenotypes of MEF cells under high glucose condition...
August 31, 2018: Aging Cell
Robert Büttner, Alexander Schulz, Michael Reuter, Asha K Akula, Thomas Mindos, Annemarie Carlstedt, Lars B Riecken, Stephan L Baader, Reinhard Bauer, Helen Morrison
The regenerative capacity of peripheral nerves declines during aging, contributing to the development of neuropathies, limiting organism function. Changes in Schwann cells prompt failures in instructing maintenance and regeneration of aging nerves; molecular mechanisms of which have yet to be delineated. Here, we identified an altered inflammatory environment leading to a defective Schwann cell response, as an underlying mechanism of impaired nerve regeneration during aging. Chronic inflammation was detected in intact uninjured old nerves, characterized by increased macrophage infiltration and raised levels of monocyte chemoattractant protein 1 (MCP1) and CC chemokine ligand 11 (CCL11)...
August 31, 2018: Aging Cell
Jéssica M Vilas, Carmen Carneiro, Sabela Da Silva-Álvarez, Alba Ferreirós, Patricia González, María Gómez, Sagrario Ortega, Manuel Serrano, Tomás García-Caballero, Miguel González-Barcia, Anxo Vidal, Manuel Collado
Aging is characterized by a gradual functional decline of tissues with age. Adult stem and progenitor cells are responsible for tissue maintenance, repair, and regeneration, but during aging, this population of cells is decreased or its activity is reduced, compromising tissue integrity and causing pathologies that increase vulnerability, and ultimately lead to death. The causes of stem cell exhaustion during aging are not clear, and whether a reduction in stem cell function is a cause or a consequence of aging remains unresolved...
August 20, 2018: Aging Cell
Nicolas Musi, Joseph M Valentine, Kathryn R Sickora, Eric Baeuerle, Cody S Thompson, Qiang Shen, Miranda E Orr
Tau protein accumulation is the most common pathology among degenerative brain diseases, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), traumatic brain injury (TBI) and over twenty others. Tau-containing neurofibrillary tangle (NFT) accumulation is the closest correlate with cognitive decline and cell loss (Arriagada et al., 1992), yet mechanisms mediating tau toxicity are poorly understood. NFT formation does not induce apoptosis (de Calignon et al., 2009), which suggests secondary mechanisms are driving toxicity...
August 20, 2018: Aging Cell
Elisabetta Mattioli, Davide Andrenacci, Cecilia Garofalo, Sabino Prencipe, Katia Scotlandi, Daniel Remondini, Davide Gentilini, Anna Maria Di Blasio, Sergio Valente, Emanuela Scarano, Lucia Cicchilitti, Giulia Piaggio, Antonello Mai, Giovanna Lattanzi
Defects in stress response are main determinants of cellular senescence and organism aging. In fibroblasts from patients affected by Hutchinson-Gilford progeria, a severe LMNA-linked syndrome associated with bone resorption, cardiovascular disorders, and premature aging, we found altered modulation of CDKN1A, encoding p21, upon oxidative stress induction, and accumulation of senescence markers during stress recovery. In this context, we unraveled a dynamic interaction of lamin A/C with HDAC2, an histone deacetylase that regulates CDKN1A expression...
August 15, 2018: Aging Cell
Dagmara McGuinness, Suhaib Mohammed, Laura Monaghan, Paul A Wilson, David B Kingsmore, Oliver Shapter, Karen S Stevenson, Shana M Coley, Luke Devey, Robert B Kirkpatrick, Paul G Shiels
Chronic kidney disease and associated comorbidities (diabetes, cardiovascular diseases) manifest with an accelerated ageing phenotype, leading ultimately to organ failure and renal replacement therapy. This process can be modulated by epigenetic and environmental factors which promote loss of physiological function and resilience to stress earlier, linking biological age with adverse outcomes post-transplantation including delayed graft function (DGF). The molecular features underpinning this have yet to be fully elucidated...
August 9, 2018: Aging Cell
Antonia Graja, Francisco Garcia-Carrizo, Anne-Marie Jank, Sabrina Gohlke, Thomas H Ambrosi, Wenke Jonas, Siegfried Ussar, Matthias Kern, Annette Schürmann, Krasimira Aleksandrova, Matthias Blüher, Tim J Schulz
Remodeling of the extracellular matrix is a key component of the metabolic adaptations of adipose tissue in response to dietary and physiological challenges. Disruption of its integrity is a well-known aspect of adipose tissue dysfunction, for instance, during aging and obesity. Adipocyte regeneration from a tissue-resident pool of mesenchymal stem cells is part of normal tissue homeostasis. Among the pathophysiological consequences of adipogenic stem cell aging, characteristic changes in the secretory phenotype, which includes matrix-modifying proteins, have been described...
August 7, 2018: Aging Cell
Shirin Elhaik Goldman, David Goez, David Last, Sharone Naor, Sigal Liraz Zaltsman, Inbal Sharvit-Ginon, Dana Atrakchi-Baranes, Chen Shemesh, Rachel Twitto-Greenberg, Shoval Tsach, Roni Lotan, Alicia Leikin-Frenkel, Aviv Shish, Yael Mardor, Michal Schnaider Beeri, Itzik Cooper
Type 2 diabetes (T2D) is associated with increased risk of Alzheimer's disease (AD). There is evidence for impaired blood-brain barrier (BBB) in both diseases, but its role in the interplay between them is not clear. Here, we investigated the effects of high-fat diet (HFD), a model for T2D, on the Tg2576 mouse model of AD, in regard to BBB function. We showed that HFD mice had higher weight, more insulin resistance, and higher serum HDL cholesterol levels, primarily in Tg2576 mice, which also had higher brain lipids content...
August 6, 2018: Aging Cell
Clara Ortega-de San Luis, Manuel A Sanchez-Garcia, Jose Luis Nieto-Gonzalez, Pablo García-Junco-Clemente, Adoracion Montero-Sanchez, Rafael Fernandez-Chacon, Alberto Pascual
The striatum integrates motor behavior using a well-defined microcircuit whose individual components are independently affected in several neurological diseases. The glial cell line-derived neurotrophic factor (GDNF), synthesized by striatal interneurons, and Sonic hedgehog (Shh), produced by the dopaminergic neurons of the substantia nigra (DA SNpc), are both involved in the nigrostriatal maintenance but the reciprocal neurotrophic relationships among these neurons are only partially understood. To define the postnatal neurotrophic connections among fast-spiking GABAergic interneurons (FS), cholinergic interneurons (ACh), and DA SNpc, we used a genetically induced mouse model of postnatal DA SNpc neurodegeneration and separately eliminated Smoothened (Smo), the obligatory transducer of Shh signaling, in striatal interneurons...
July 30, 2018: Aging Cell
Ryuta Mikawa, Yohei Suzuki, Hario Baskoro, Kazuki Kanayama, Kazushi Sugimoto, Tadashi Sato, Masataka Sugimoto
Senescent cells accumulate in tissues during aging and are considered to underlie several aging-associated phenotypes and diseases. We recently reported that the elimination of p19ARF -expressing senescent cells from lung tissue restored tissue function and gene expression in middle-aged (12-month-old) mice. The aging of lung tissue increases the risk of pulmonary diseases such as emphysema, and cellular senescence is accelerated in emphysema patients. However, there is currently no direct evidence to show that cellular senescence promotes the pathology of emphysema, and the involvement of senescence in the development of this disease has yet to be clarified...
July 30, 2018: Aging Cell
Yajing Peng, Samantha L Shapiro, Varuna C Banduseela, Inca A Dieterich, Kyle J Hewitt, Emery H Bresnick, Guangyao Kong, Jing Zhang, Kathryn L Schueler, Mark P Keller, Alan D Attie, Timothy A Hacker, Ruth Sullivan, Elle Kielar-Grevstad, Sebastian I Arriola Apelo, Dudley W Lamming, Rozalyn M Anderson, Luigi Puglielli
The membrane transporter AT-1/SLC33A1 translocates cytosolic acetyl-CoA into the lumen of the endoplasmic reticulum (ER), participating in quality control mechanisms within the secretory pathway. Mutations and duplication events in AT-1/SLC33A1 are highly pleiotropic and have been linked to diseases such as spastic paraplegia, developmental delay, autism spectrum disorder, intellectual disability, propensity to seizures, and dysmorphism. Despite these known associations, the biology of this key transporter is only beginning to be uncovered...
July 27, 2018: Aging Cell
Lakshmi Narayanan Lakshmanan, Zhuangli Yee, Li Fang Ng, Rudiyanto Gunawan, Barry Halliwell, Jan Gruber
Disruption of mitochondrial metabolism and loss of mitochondrial DNA (mtDNA) integrity are widely considered as evolutionarily conserved (public) mechanisms of aging (López-Otín et al., Cell, 153, 2013 and 1194). Human aging is associated with loss in skeletal muscle mass and function (Sarcopenia), contributing significantly to morbidity and mortality. Muscle aging is associated with loss of mtDNA integrity. In humans, clonally expanded mtDNA deletions colocalize with sites of fiber breakage and atrophy in skeletal muscle...
July 24, 2018: Aging Cell
Joan Villarroya, José M Gallego-Escuredo, Alejando Delgado-Anglés, Montserrat Cairó, Ricardo Moure, Ma Gracia Mateo, Joan C Domingo, Pere Domingo, Marta Giralt, Francesc Villarroya
Fibroblast growth factor 21 (FGF21) has been proposed to be an antiaging hormone on the basis of experimental studies in rodent models. However, circulating FGF21 levels are increased with aging in rodents and humans. Moreover, despite the metabolic health-promoting effects of FGF21, the levels of this hormone are increased under conditions such as obesity and diabetes, an apparent incongruity that has been attributed to altered tissue responsiveness to FGF21. Here, we investigated serum FGF21 levels and expression of genes encoding components of the FGF21-response molecular machinery in adipose tissue from healthy elderly individuals (≥70 years old) and young controls...
July 24, 2018: Aging Cell
Emiliano Zamponi, Nahuel Zamponi, Pinar Coskun, Gonzalo Quassollo, Alfredo Lorenzo, Sergio A Cannas, Gustavo Pigino, Dante Chialvo, Katheleen Gardiner, Jorge Busciglio, Pablo Helguera
Mounting evidence implicates chronic oxidative stress as a critical driver of the aging process. Down syndrome (DS) is characterized by a complex phenotype, including early senescence. DS cells display increased levels of reactive oxygen species (ROS) and mitochondrial structural and metabolic dysfunction, which are counterbalanced by sustained Nrf2-mediated transcription of cellular antioxidant response elements (ARE). Here, we show that caspase 3/PKCδdependent activation of the Nrf2 pathway in DS and Dp16 (a mouse model of DS) cells is necessary to protect against chronic oxidative damage and to preserve cellular functionality...
July 20, 2018: Aging Cell
Andreas Patsalos, Zoltan Simandi, Tristan T Hays, Matthew Peloquin, Matine Hajian, Isabella Restrepo, Paul M Coen, Alan J Russell, Laszlo Nagy
Tissue regeneration is a highly coordinated process with sequential events including immune cell infiltration, clearance of damaged tissues, and immune-supported regrowth of the tissue. Aging has a well-documented negative impact on this process globally; however, whether changes in immune cells per se are contributing to the decline in the body's ability to regenerate tissues with aging is not clearly understood. Here, we set out to characterize the dynamics of macrophage infiltration and their functional contribution to muscle regeneration by comparing young and aged animals upon acute sterile injury...
July 12, 2018: Aging Cell
Jessica Brunquell, Rachel Raynes, Philip Bowers, Stephanie Morris, Alana Snyder, Doreen Lugano, Andrew Deonarine, Sandy D Westerheide
Defects in protein quality control during aging are central to many human diseases, and strategies are needed to better understand mechanisms of controlling the quality of the proteome. The heat-shock response (HSR) is a conserved survival mechanism mediated by the transcription factor HSF1 which functions to maintain proteostasis. In mammalian cells, HSF1 is regulated by a variety of factors including the prolongevity factor SIRT1. SIRT1 promotes the DNA-bound state of HSF1 through deacetylation of the DNA-binding domain of HSF1, thereby enhancing the HSR...
July 12, 2018: Aging Cell
Rachel Stegeman, Hana Hall, Spencer E Escobedo, Henry C Chang, Vikki M Weake
Changes in splicing patterns are a characteristic of the aging transcriptome; however, it is unclear whether these age-related changes in splicing facilitate the progressive functional decline that defines aging. In Drosophila, visual behavior declines with age and correlates with altered gene expression in photoreceptors, including downregulation of genes encoding splicing factors. Here, we characterized the significance of these age-regulated splicing-associated genes in both splicing and visual function...
July 12, 2018: Aging Cell
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