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  • 1
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    Autophagy maintains stemness by preventing senescence (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-01-08
    Description: During ageing, muscle stem-cell regenerative function declines. At advanced geriatric age, this decline is maximal owing to transition from a normal quiescence into an irreversible senescence state. How satellite cells maintain quiescence and avoid senescence until advanced age remains unknown. Here we report that basal autophagy is essential to maintain the stem-cell quiescent state in mice. Failure of autophagy in physiologically aged satellite cells or genetic impairment of autophagy in young cells causes entry into senescence by loss of proteostasis, increased mitochondrial dysfunction and oxidative stress, resulting in a decline in the function and number of satellite cells. Re-establishment of autophagy reverses senescence and restores regenerative functions in geriatric satellite cells. As autophagy also declines in human geriatric satellite cells, our findings reveal autophagy to be a decisive stem-cell-fate regulator, with implications for fostering muscle regeneration in sarcopenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia-Prat, Laura -- Martinez-Vicente, Marta -- Perdiguero, Eusebio -- Ortet, Laura -- Rodriguez-Ubreva, Javier -- Rebollo, Elena -- Ruiz-Bonilla, Vanessa -- Gutarra, Susana -- Ballestar, Esteban -- Serrano, Antonio L -- Sandri, Marco -- Munoz-Canoves, Pura -- England -- Nature. 2016 Jan 7;529(7584):37-42. doi: 10.1038/nature16187.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), CIBER on Neurodegenerative diseases (CIBERNED), E-08003 Barcelona, Spain. ; Neurodegenerative Diseases Research Group, Vall d'Hebron Research Institute-CIBERNED, E-08035 Barcelona, Spain. ; Chromatin and Disease Group, Cancer Epigenetics and Biology Programme (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, E-08907 Barcelona, Spain. ; Advanced Fluorescence Microscopy Unit, Molecular Biology Institute of Barcelona (IBMB-CSIC), E-08028 Barcelona, Spain. ; Department of Biomedical Science, University of Padova, 35100 Padova, Italy. ; Telethon Institute of Genetics and Medicine (TIGEM), 80131 Napoli, Italy. ; ICREA, E-08908 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26738589" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/pathology ; Animals ; Autophagy/*physiology ; *Cell Aging ; Cell Count ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Epigenesis, Genetic ; Homeostasis ; Humans ; Male ; Mice ; Mitochondria/metabolism/pathology ; Mitochondrial Degradation ; Muscle, Skeletal/cytology/pathology ; Organelles/metabolism ; Oxidative Stress ; Proteins/metabolism ; Reactive Oxygen Species/metabolism ; Regeneration ; Sarcopenia/pathology/prevention & control ; Satellite Cells, Skeletal Muscle/*cytology/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Modelling a light-driven phytoplankton succession (2014)
    Oxford University Press
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    Publication Date: 2014-01-10
    Description: We used a numerical model to investigate if and to what extent cellular photoprotective capacity accounts for succession and vertical distribution of marine phytoplankton species/groups. A model describing xanthophyll photoprotective activity in phytoplankton has been implemented in the European Regional Sea Ecosystem Model and applied at the station L4 in the Western English Channel. Primary producers were subdivided into three phytoplankton functional types defined in terms of their capacity to acclimate to different light-specific environments: low light (LL-type), high light (HL-type) and variable light (VL-type) adapted species. The LL-type is assumed to have low cellular level of xanthophyll-cycling pigments (PX) relative to the modelled photosynthetically active pigments (chlorophyll and fucoxanthin (FUCO) = PSP). The HL-type has high PX content relative to PSP while VL-type presents an intermediate PX to PSP ratio. Furthermore, the VL-type is capable of reversibly converting FUCO to PX and synthesizing new PX under high-light stress. In order to reproduce phytoplankton community succession with each of the three groups being dominant in different periods of the year, we had also to assume reduced grazing pressure on HL-adapted species. Model simulations realistically reproduce the observed seasonal patterns of pigments and nutrients highlighting the reasonability of the underpinning assumptions. Our model suggests that pigment-mediated photophysiology plays a primary role in determining the evolution of marine phytoplankton communities in the winter-spring period corresponding to the shoaling of the mixed layer and the increase of light intensity. Grazing selectivity however contributes to the phytoplankton community composition in summer.
    Print ISSN: 0142-7873
    Electronic ISSN: 1464-3774
    Topics: Biology
    Published by Oxford University Press
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  • 3
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    Loss of P-type ATPase ATP13A2/PARK9 function induces general lysosomal deficiency and leads to Parkinson disease neurodegeneration (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-05-30
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    ATP13A2 promotes lysosomal deficiency [Neuroscience] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-06-13
    Description: Parkinson disease (PD) is a progressive neurodegenerative disorder pathologically characterized by the loss of dopaminergic neurons from the substantia nigra pars compacta and the presence, in affected brain regions, of protein inclusions named Lewy bodies (LBs). The ATP13A2 gene (locus PARK9) encodes the protein ATP13A2, a lysosomal type 5 P-type ATPase that is linked to autosomal recessive familial parkinsonism. The physiological function of ATP13A2, and hence its role in PD, remains to be elucidated. Here, we show that PD-linked mutations in ATP13A2 lead to several lysosomal alterations in ATP13A2 PD patient-derived fibroblasts, including impaired lysosomal acidification, decreased proteolytic processing of lysosomal enzymes, reduced degradation of lysosomal substrates, and diminished lysosomal-mediated clearance of autophagosomes. Similar alterations are observed in stable ATP13A2-knockdown dopaminergic cell lines, which are associated with cell death. Restoration of ATP13A2 levels in ATP13A2-mutant/depleted cells restores lysosomal function and attenuates cell death. Relevant to PD, ATP13A2 levels are decreased in dopaminergic nigral neurons from patients with PD, in which ATP13A2 mostly accumulates within Lewy bodies. Our results unravel an instrumental role of ATP13A2 deficiency on lysosomal function and cell viability and demonstrate the feasibility and therapeutic potential of modulating ATP13A2 levels in the context of PD.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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