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      NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice.

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          Abstract

          Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD(+)) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD(+) precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmd(mdx)/J) mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs and melanocyte SCs and increases mouse life span. Strategies that conserve cellular NAD(+) may reprogram dysfunctional SCs and improve life span in mammals.

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          OpenSWATH enables automated, targeted analysis of data-independent acquisition MS data.

          Hannes L. Röst, George Rosenberger, Pedro Cabrera Navarro … (2014)
          Article 0 comments Cited 270 times – based on 0 reviews     Review now
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            Metabolic plasticity in stem cell homeostasis and differentiation.

            Clifford D L Folmes, Petras Dzeja, Timothy Nelson … (2012)
            Plasticity in energy metabolism allows stem cells to match the divergent demands of self-renewal and lineage specification. Beyond a role in energetic support, new evidence implicates nutrient-responsive metabolites as mediators of crosstalk between metabolic flux, cellular signaling, and epigenetic regulation of cell fate. Stem cell metabolism also offers a potential target for controlling tissue homeostasis and regeneration in aging and disease. In this Perspective, we cover recent progress establishing an emerging relationship between stem cell metabolism and cell fate control. Copyright © 2012 Elsevier Inc. All rights reserved.
            Article 0 comments Cited 239 times – based on 0 reviews     Review now
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              Is Open Access

              Chromatin Modifications as Determinants of Muscle Stem Cell Quiescence and Chronological Aging

              Ling Liu, Tom Cheung, Gregory Charville … (2013)
              Summary The ability to maintain quiescence is critical for the long-term maintenance of a functional stem cell pool. To date, the epigenetic and transcriptional characteristics of quiescent stem cells and how they change with age remain largely unknown. In this study, we explore the chromatin features of adult skeletal muscle stem cells, or satellite cells (SCs), which reside predominantly in a quiescent state in fully developed limb muscles of both young and aged mice. Using a ChIP-seq approach to obtain global epigenetic profiles of quiescent SCs (QSCs), we show that QSCs possess a permissive chromatin state in which few genes are epigenetically repressed by Polycomb group (PcG)-mediated histone 3 lysine 27 trimethylation (H3K27me3), and a large number of genes encoding regulators that specify nonmyogenic lineages are demarcated by bivalent domains at their transcription start sites (TSSs). By comparing epigenetic profiles of QSCs from young and old mice, we also provide direct evidence that, with age, epigenetic changes accumulate and may lead to a functional decline in quiescent stem cells. These findings highlight the importance of chromatin mapping in understanding unique features of stem cell identity and stem cell aging.
              Article 0 comments Cited 221 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Science
                Title: Science (New York, N.Y.)
                ISSN (Electronic): 1095-9203
                ISSN (Print): 0036-8075
                Publication date (Electronic): Jun 17 2016
                Volume: 352
                Issue: 6292
                Affiliations
                [1 ] Laboratory of Integrative and Systems Physiology, École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
                [2 ] Department of Biology, Institute of Molecular Systems Biology, Eidgenössische Technische Hochschule Zürich (ETHZ), 8093 Zurich, Switzerland.
                [3 ] Laboratory of Integrative and Systems Physiology, École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland. Laboratory of Molecular Biology of Exercise, School of Applied Science, University of Campinas, CEP 13484-350 Limeira, São Paulo, Brazil.
                [4 ] Laboratory of Stem Cell Bioengineering, EPFL, 1015 Lausanne, Switzerland.
                [5 ] Department of Biology, Institute of Molecular Systems Biology, Eidgenössische Technische Hochschule Zürich (ETHZ), 8093 Zurich, Switzerland. Faculty of Science, University of Zurich, 8057 Zurich, Switzerland.
                [6 ] Metabolic Signaling, EPFL, 1015 Lausanne, Switzerland.
                [7 ] Laboratory of Integrative and Systems Physiology, École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland. Interdisciplinary School of Health Sciences, University of Ottawa Brain and Mind Research Institute, 451 Smyth Road, K1H 8M5 Ottawa, Ontario, Canada. kmenzies@uottawa.ca admin.auwerx@epfl.ch.
                [8 ] Laboratory of Integrative and Systems Physiology, École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland. kmenzies@uottawa.ca admin.auwerx@epfl.ch.
                Article
                Publisher Item ID: science.aaf2693
                DOI: 10.1126/science.aaf2693
                PubMed ID: 27127236
                SO-VID: df7caa78-2a25-4619-8780-7774904f8f58
                Copyright © Copyright © 2016, American Association for the Advancement of Science.
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