Open AccessBrief Report: Long‐Term Functional Engraftment of Mesenchymal Progenitor Cells in a Mouse Model of Accelerated Aging
Author(s) -
Singh Lakshman,
Brennan Tracy A.,
Kim JungHoon,
Egan Kevin P.,
Mcmillan Emily A.,
Chen Qijun,
Hankenson Kurt D.,
Zhang Yi,
Emerson Stephen G.,
Johnson F. Brad,
Pignolo Robert J.
Publication year - 2013
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.1294
Subject(s) - mesenchymal stem cell , biology , progenitor cell , osteoblast , senile osteoporosis , telomere , bone marrow , senescence , cancer research , microbiology and biotechnology , progenitor , phenotype , osteoporosis , transplantation , stem cell , immunology , endocrinology , medicine , genetics , in vitro , dna , gene
Age‐related osteoporosis is characterized by a decrease in bone‐forming capacity mediated by defects in the number and function of osteoblasts. An important cellular mechanism that may in part explain osteoblast dysfunction that occurs with aging is senescence of mesenchymal progenitor cells (MPCs). In the telomere‐based Wrn −/− Terc −/− model of accelerated aging, the osteoporotic phenotype of these mice is also associated with a major decline in MPC differentiation into osteoblasts. To investigate the role of MPC aging as a cell‐autonomous mechanism in senile bone loss, transplantation of young wild‐type whole bone marrow into Wrn −/− Terc −/− mutants was performed and the ability of engrafted cells to differentiate into cells of the osteoblast lineage was assessed. We found that whole bone marrow transplantation in Wrn −/− Terc −/− mice resulted in functional engraftment of MPCs up to 42 weeks, which was accompanied by a survival advantage as well as delays in microarchitectural features of skeletal aging. S TEM C ELLS 2013;31:607–611