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  • 1
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    Geriatric muscle stem cells switch reversible quiescence into senescence (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-02-14
    Description: Regeneration of skeletal muscle depends on a population of adult stem cells (satellite cells) that remain quiescent throughout life. Satellite cell regenerative functions decline with ageing. Here we report that geriatric satellite cells are incapable of maintaining their normal quiescent state in muscle homeostatic conditions, and that this irreversibly affects their intrinsic regenerative and self-renewal capacities. In geriatric mice, resting satellite cells lose reversible quiescence by switching to an irreversible pre-senescence state, caused by derepression of p16(INK4a) (also called Cdkn2a). On injury, these cells fail to activate and expand, undergoing accelerated entry into a full senescence state (geroconversion), even in a youthful environment. p16(INK4a) silencing in geriatric satellite cells restores quiescence and muscle regenerative functions. Our results demonstrate that maintenance of quiescence in adult life depends on the active repression of senescence pathways. As p16(INK4a) is dysregulated in human geriatric satellite cells, these findings provide the basis for stem-cell rejuvenation in sarcopenic muscles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sousa-Victor, Pedro -- Gutarra, Susana -- Garcia-Prat, Laura -- Rodriguez-Ubreva, Javier -- Ortet, Laura -- Ruiz-Bonilla, Vanessa -- Jardi, Merce -- Ballestar, Esteban -- Gonzalez, Susana -- Serrano, Antonio L -- Perdiguero, Eusebio -- Munoz-Canoves, Pura -- England -- Nature. 2014 Feb 20;506(7488):316-21. doi: 10.1038/nature13013. Epub 2014 Feb 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University, CIBER on Neurodegenerative diseases, E-08003 Barcelona, Spain [2] Buck Institute for Research on Aging, Novato, California 94945, USA. ; 1] Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University, CIBER on Neurodegenerative diseases, E-08003 Barcelona, Spain [2]. ; Chromatin and Disease Group, Cancer Epigenetics and Biology Programme, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, E-08907 Barcelona, Spain. ; Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University, CIBER on Neurodegenerative diseases, E-08003 Barcelona, Spain. ; Stem Cell Aging Group, Centro Nacional de Investigaciones Cardiovasculares, E-28029 Madrid, Spain. ; 1] Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University, CIBER on Neurodegenerative diseases, E-08003 Barcelona, Spain [2] Institucio Catalana de Recerca i Estudis Avancats, E-08010 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24522534" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aging/*metabolism ; Animals ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/*metabolism ; E2F1 Transcription Factor/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Progeria/metabolism/pathology ; Regeneration ; Rejuvenation ; Retinoblastoma Protein/metabolism ; Satellite Cells, Skeletal Muscle/*cytology/*metabolism ; Young Adult
    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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    Autophagy maintains stemness by preventing senescence (2016)
    Nature Publishing Group (NPG)
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    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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  • 3
    Electronic Resource
    Electronic Resource
    The plasminogen activator system: biology and regulation (1999)
    Springer
    Cellular and molecular life sciences 56 (1999), S. 104-132 
    Details
    ISSN: 1420-9071
    Keywords: Key words. Cell invasion; cell motility; fibrinolysis; metastasis; mRNA stability; plasminogen activator; plasminogen activator inhibitor; signal transduction; transcriptional regulation; uPA receptor.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. The regulation of plasminogen activation involves genes for two plasminogen activators (tissue type and urokinase type), two specific inhibitors (type 1 and type 2), and a membrane-anchored urokinase-type plasminogen-activator-specific receptor. This system plays an important role in various biological processes involving extracellular proteolysis. Recent studies have revealed that the system, through interplay with integrins and the extracellular matrix protein vitronectin, is also involved in the regulation of cell migration and proliferation in a manner independent of proteolytic activity. The genes are expressed in many different cell types and their expression is under the control of diverse extracellular signals. Gene expression reflects the levels of the corresponding mRNA, which should be the net result of synthesis and degradation. Thus, modulation of mRNA stability is an important factor in overall regulation. This review summarizes current understanding of the biology and regulation of genes involved in plasminogen activation at different levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00000615
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  • 4
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    Amelioration of Duchenne muscular dystrophy in mdx mice by elimination of matrix-associated fibrin-driven inflammation coupled to the {alpha}M{beta}2 leukocyte integrin receptor (2012)
    Oxford University Press
    Details
    Publication Date: 2012-04-12
    Description: In Duchenne muscular dystrophy (DMD), a persistently altered and reorganizing extracellular matrix (ECM) within inflamed muscle promotes damage and dysfunction. However, the molecular determinants of the ECM that mediate inflammatory changes and faulty tissue reorganization remain poorly defined. Here, we show that fibrin deposition is a conspicuous consequence of muscle-vascular damage in dystrophic muscles of DMD patients and mdx mice and that elimination of fibrin(ogen) attenuated dystrophy progression in mdx mice. These benefits appear to be tied to: (i) a decrease in leukocyte integrin α M β 2 -mediated proinflammatory programs, thereby attenuating counterproductive inflammation and muscle degeneration; and (ii) a release of satellite cells from persistent inhibitory signals, thereby promoting regeneration. Remarkably, Fib-gamma(390-396A) (Fib 390-396A ) mice expressing a mutant form of fibrinogen with normal clotting function, but lacking the α M β 2 binding motif, ameliorated dystrophic pathology. Delivery of a fibrinogen/α M β 2 blocking peptide was similarly beneficial. Conversely, intramuscular fibrinogen delivery sufficed to induce inflammation and degeneration in fibrinogen-null mice. Thus, local fibrin(ogen) deposition drives dystrophic muscle inflammation and dysfunction, and disruption of fibrin(ogen)-α M β 2 interactions may provide a novel strategy for DMD treatment.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 5
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    The plasminogen activator system: biology and regulation (1999)
    Springer
    Details
    Publication Date: 1999-10-01
    Print ISSN: 1420-682X
    Electronic ISSN: 1420-9071
    Topics: Biology , Medicine
    Published by Springer
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  • 6
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    Restoration of muscle strength in dystrophic muscle by angiotensin-1-7 through inhibition of TGF-{beta} signalling (2014)
    Oxford University Press
    Details
    Publication Date: 2014-02-08
    Description: Duchenne muscular dystrophy (DMD) is the most common inherited neuromuscular disease, and is characterized by the lack of dystrophin, muscle wasting, increased transforming growth factor (TGF)-β Smad-dependent signalling and fibrosis. Acting via the Mas receptor, angiotensin-1-7 [Ang-(1-7)], is part of the renin–angiotensin system, with the opposite effect to that of angiotensin II. We hypothesized that the Ang-(1-7)/Mas receptor axis might protect chronically damaged tissues as in skeletal muscle of the DMD mouse model mdx . Infusion or oral administration of Ang-(1-7) in mdx mice normalized skeletal muscle architecture, decreased local fibrosis and improved muscle function in vitro and in vivo . These positive effects were mediated by the inhibition of TGF-β Smad signalling, which in turn led to reduction of the pro-fibrotic microRNA miR-21 concomitant with a reduction in the number of TCF4 expressing fibroblasts. Mdx mice infused with Mas antagonist (A-779) and mdx deficient for the Mas receptor showed highly deteriorated muscular architecture, increased fibrosis and TGF-β signalling with diminished muscle strength. These results suggest that this novel compound Ang-(1-7) might be used to improve quality of life and delay death in individuals with DMD and this drug should be investigated in further pre-clinical trials.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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