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<i>Sostdc1</i> deficiency accelerates fracture healing by promoting the expansion of periosteal mesenchymal stem cells [Sostdc1 Participates in Bone Maintenance and Fracture Repair] [electronic resource].

Published
Washington, D.C. : United States. Dept. of Energy, 2016.
Oak Ridge, Tenn. : Distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy
Physical Description
PDF-file: 32 pages; size: 2.5 Mbytes
Additional Creators
Lawrence Berkeley National Laboratory, United States. Department of Energy, and United States. Department of Energy. Office of Scientific and Technical Information
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Summary
Loss of Sostdc1, a growth factor paralogous to Sost, causes the formation of ectopic incisors, fused molars, abnormal hair follicles, and resistance to kidney disease. Sostdc1 is expressed in the periosteum, a source of osteoblasts, fibroblasts and mesenchymal progenitor cells, which are critically important for fracture repair. Here, we investigated the role of Sostdc1 in bone metabolism and fracture repair. Mice lacking Sostdc1 (Sostdc1–/–) had a low bone mass phenotype associated with loss of trabecular bone in both lumbar vertebrae and in the appendicular skeleton. In contrast, Sostdc1–/– cortical bone measurements revealed larger bones with higher BMD, suggesting that Sostdc1 exerts differential effects on cortical and trabecular bone. Mid-diaphyseal femoral fractures induced in Sostdc1–/– mice showed that the periosteal population normally positive for Sostdc1 rapidly expands during periosteal thickening and these cells migrate into the fracture callus at 3 days post fracture. Quantitative analysis of mesenchymal stem cell (MSC) and osteoblast populations determined that MSCs express Sostdc1, and that Sostdc1–/– 5 day calluses harbor > 2-fold more MSCs than fractured wildtype controls. Histologically a fraction of Sostdc1-positive cells also expressed nestin and α-smooth muscle actin, suggesting that Sostdc1 marks a population of osteochondral progenitor cells that actively participate in callus formation and bone repair. Elevated numbers of MSCs in D5 calluses resulted in a larger, more vascularized cartilage callus at day 7, and a more rapid turnover of cartilage with significantly more remodeled bone and a thicker cortical shell at 21 days post fracture. In conclusion, these data support accelerated or enhanced bone formation/remodeling of the callus in Sostdc1–/– mice, suggesting that Sostdc1 may promote and maintain mesenchymal stem cell quiescence in the periosteum.
Report Numbers
E 1.99:llnl-jrnl-658875
llnl-jrnl-658875
Subject(s)
Note
Published through SciTech Connect.
04/19/2016.
"llnl-jrnl-658875"
Bone 88 C ISSN 8756-3282 AM
Nicole M. Collette; Cristal S. Yee; Nicholas R. Hum; Deepa K. Murugesh; Blaine A. Christiansen; LiQin Xie; Aris N. Economides; Jennifer O. Manilay; Alexander G. Robling; Gabriela G. Loots.
Funding Information
AC52-07NA27344
View MARC record | catkey: 23497925