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Title: Age-related impairment of mesenchymal progenitor cell function
Authors: Stolzing, Alexandra
Scutt, Andrew
Keywords: Aging
Fibroblast colony-forming unit (CFU-f)
Mesenchymal progenitor
Oxidative stress
Issue Date: 2006
Publisher: © The Authors; Journal compilation © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland
Citation: STOLZING, A. and SCUTT, A., 2006. Age-related impairment of mesenchymal progenitor cell function. Aging Cell, 5 (3), pp. 213 - 224.
Abstract: In most mesenchymal tissues a subcompartment of multipotent progenitor cells is responsible for the maintenance and repair of the tissue following trauma. With increasing age, the ability of tissues to repair themselves is diminished, which may be due to reduced functional capacity of the progenitor cells. The purpose of this study was to investigate the effect of aging on rat mesenchymal progenitor cells. Mesenchymal progenitor cells were isolated from Wistar rats aged 3, 7, 12 and 56 weeks. Viability, capacity for differentiation and cellular aging were examined. Cells from the oldest group accumulated raised levels of oxidized proteins and lipids and showed decreased levels of antioxidative enzyme activity. This was reflected in decreased fibroblast colony-forming unit (CFU-f) numbers, increased levels of apoptosis and reduced proliferation and potential for differentiation. These data suggest that the reduced ability to maintain mesenchymal tissue homeostasis in aged mammals is not purely due to a decline in progenitor cells numbers but also to a loss of progenitor functionality due to the accumulation of oxidative damage, which may in turn be a causative factor in a number of age-related pathologies such as arthritis, tendinosis and osteoporosis. © 2006 The Authors Journal compilation © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2006.
Description: This is the accepted version of the following article: STOLZING, A. and SCUTT, A., 2006. Age-related impairment of mesenchymal progenitor cell function. Aging Cell, 5 (3), pp. 213 - 224., which has been published in final form at http://dx.doi.org/10.1111/j.1474-9726.2006.00213.x
Sponsor: BBSRC
Version: Accepted for publication
DOI: 10.1111/j.1474-9726.2006.00213.x
URI: https://dspace.lboro.ac.uk/2134/16871
Publisher Link: http://dx.doi.org/10.1111/j.1474-9726.2006.00213.x
ISSN: 1474-9718
Appears in Collections:Published Articles (Mechanical, Electrical and Manufacturing Engineering)

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