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  • Fibroblasts/cytology/physiology  (1)
  • American Association for the Advancement of Science (AAAS)  (1)
  • 1
    Publication Date: 2007-08-11
    Description: The regenerative potential of skeletal muscle declines with age, and this impairment is associated with an increase in tissue fibrosis. We show that muscle stem cells (satellite cells) from aged mice tend to convert from a myogenic to a fibrogenic lineage as they begin to proliferate and that this conversion is mediated by factors in the systemic environment of the old animals. We also show that this lineage conversion is associated with an activation of the canonical Wnt signaling pathway in aged myogenic progenitors and can be suppressed by Wnt inhibitors. Furthermore, components of serum from aged mice that bind to the Frizzled family of proteins, which are Wnt receptors, may account for the elevated Wnt signaling in aged cells. These results indicate that the Wnt signaling pathway may play a critical role in tissue-specific stem cell aging and an increase in tissue fibrosis with age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brack, Andrew S -- Conboy, Michael J -- Roy, Sudeep -- Lee, Mark -- Kuo, Calvin J -- Keller, Charles -- Rando, Thomas A -- AG23806/AG/NIA NIH HHS/ -- DK069989/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 10;317(5839):807-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17690295" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Cell Aging/*physiology ; Cell Lineage ; Cell Proliferation ; Fibroblasts/cytology/physiology ; Fibrosis/*pathology ; Frizzled Receptors/metabolism ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/cytology/metabolism/*pathology ; Parabiosis ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology/*physiology ; *Signal Transduction ; Wnt Proteins/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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