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1000 Titel
  • MicroRNA miR-29 controls a compensatory response to limit neuronal iron accumulation during adult life and aging
1000 Autor/in
  1. Ripa, Roberto |
  2. Dolfi, Luca |
  3. TERRIGNO, MARCO |
  4. Pandolfini, Luca |
  5. Savino, Aurora |
  6. Arcucci, Valeria |
  7. Groth, Marco |
  8. Terzibasi Tozzini, Eva |
  9. Baumgart, Mario |
  10. Cellerino, Alessandro |
1000 Erscheinungsjahr 2017
1000 LeibnizOpen
1000 Art der Datei
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2017-02-13
1000 Erschienen in
1000 Quellenangabe
  • 15:9
1000 FRL-Sammlung
1000 Copyrightjahr
  • 2017
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.1186/s12915-017-0354-x |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/28193224/ |
1000 Ergänzendes Material
  • https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-017-0354-x#Decs |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • BACKGROUND: A widespread modulation of gene expression occurs in the aging brain, but little is known as to the upstream drivers of these changes. MicroRNAs emerged as fine regulators of gene expression in many biological contexts and they are modulated by age. MicroRNAs may therefore be part of the upstream drivers of the global gene expression modulation correlated with aging and aging-related phenotypes. RESULTS: Here, we show that microRNA-29 (miR-29) is induced during aging in short-lived turquoise killifish brain and genetic antagonism of its function induces a gene-expression signature typical of aging. Mechanicistically, we identified Ireb2 (a master gene for intracellular iron delivery that encodes for IRP2 protein), as a novel miR-29 target. MiR-29 is induced by iron loading and, in turn, it reduces IRP2 expression in vivo, therefore limiting intracellular iron delivery in neurons. Genetically modified fish with neuro-specific miR-29 deficiency exhibit increased levels of IRP2 and transferrin receptor, increased iron content, and oxidative stress. CONCLUSIONS: Our results demonstrate that age-dependent miR-29 upregulation is an adaptive mechanism that counteracts the expression of some aging-related phenotypes and its anti-aging activity is primarily exerted by regulating intracellular iron homeostasis limiting excessive iron-exposure in neurons.
1000 Sacherschließung
lokal KEGG Pathway Analysis
lokal Iron Homeostasis
lokal Iron Accumulation
lokal Multisite Gateway
lokal Dietary Iron Supplementation
1000 Fachgruppe
  1. Medizin |
  2. Biologie |
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/creator/UmlwYSwgUm9iZXJ0bw==|https://frl.publisso.de/adhoc/creator/RG9sZmksIEx1Y2E=|https://orcid.org/0000-0001-8967-7269|https://orcid.org/0000-0003-1444-8167|https://frl.publisso.de/adhoc/creator/U2F2aW5vLCBBdXJvcmE=|https://frl.publisso.de/adhoc/creator/QXJjdWNjaSwgVmFsZXJpYQ==|https://orcid.org/0000-0002-9199-8990|https://orcid.org/0000-0003-3317-1538|https://orcid.org/0000-0001-8172-1595|https://orcid.org/0000-0003-3834-0097
1000 Förderer
  1. Scuola Normale Superiore |
  2. Bundesamt für Bildung und Forschung (BMBF) |
1000 Fördernummer
  1. -
  2. 0315581A
1000 Förderprogramm
  1. Internal gran
  2. JenAge
1000 Dateien
1000 Förderung
  1. 1000 joinedFunding-child
    1000 Förderer Scuola Normale Superiore |
    1000 Förderprogramm Internal gran
    1000 Fördernummer -
  2. 1000 joinedFunding-child
    1000 Förderer Bundesamt für Bildung und Forschung (BMBF) |
    1000 Förderprogramm JenAge
    1000 Fördernummer 0315581A
1000 Objektart article
1000 Beschrieben durch
1000 @id frl:6413738.rdf
1000 Erstellt am 2019-04-02T15:37:47.317+0200
1000 Erstellt von 285
1000 beschreibt frl:6413738
1000 Bearbeitet von 25
1000 Zuletzt bearbeitet Mon Apr 08 12:12:29 CEST 2019
1000 Objekt bearb. Mon Apr 08 12:12:04 CEST 2019
1000 Vgl. frl:6413738
1000 Oai Id
  1. oai:frl.publisso.de:frl:6413738 |
1000 Sichtbarkeit Metadaten public
1000 Sichtbarkeit Daten public
1000 Gegenstand von

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