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dc.contributor.authorChakkalakal, Joe V.
dc.contributor.authorJones, Kieran M.
dc.contributor.authorBasson, M. Albert
dc.contributor.authorBrack, Andrew Stephen
dc.date.accessioned2013-10-17T14:22:47Z
dc.date.issued2012
dc.identifier.citationChakkalakal, Joe V., Kieran M. Jones, M. Albert Basson, and Andrew S. Brack. 2012. The aged niche disrupts muscle stem cell quiescence. Nature 490(7420): 355-360.en_US
dc.identifier.issn0028-0836en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:11180414
dc.description.abstractSUMMARY The niche is a conserved regulator of stem cell quiescence and function. During aging, stem cell function declines. To what extent and by which means age-related changes within the niche contribute to this phenomenon are unknown. We demonstrate that the aged muscle stem cell niche, the muscle fiber, expresses FGF2 under homeostatic conditions, driving a subset of satellite cells to break quiescence and lose self-renewing capacity. We show that relatively dormant aged satellite cells robustly express Sprouty1 (spry1), an inhibitor of FGF signalling. Increasing FGF signalling in aged satellite cells under homeostatic conditions by removing spry1, results in the loss of quiescence, satellite cell depletion and diminished regenerative capacity. Conversely, reducing niche-derived FGF activity through inhibition of FGFR1 signalling or overexpression of spry1 in satellite cells prevents their depletion. These experiments identify an age-dependent change in the stem cell niche that directly influences stem cell quiescence and function.en_US
dc.language.isoen_USen_US
dc.relation.isversionofdoi:10.1038/nature11438en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605795/pdf/en_US
dash.licenseLAA
dc.titleThe aged niche disrupts muscle stem cell quiescenceen_US
dc.typeJournal Articleen_US
dc.description.versionAccepted Manuscripten_US
dc.relation.journalNatureen_US
dash.depositing.authorBrack, Andrew Stephen
dc.date.available2013-10-17T14:22:47Z
dc.identifier.doi10.1038/nature11438*
dash.contributor.affiliatedBrack, Andrew S


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