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• W1986543403 endingPage "e97035" @default.
• W1986543403 startingPage "e97035" @default.
• W1986543403 abstract "Host blood circulating stem cells are an important cell source that participates in the repair of damaged tissues. The clinical challenge is how to improve the recruitment of circulating stem cells into the local wound area and enhance tissue regeneration. Stromal-derived factor-1 (SDF-1) has been shown to be a potent chemoattractant of blood circulating stem cells into the local wound microenvironment. In order to investigate effects of SDF-1 on bone development and the repair of a large bone defect beyond host self-repair capacity, the BMP-induced subcutaneous ectopic bone formation and calvarial critical-sized defect murine models were used in this preclinical study. A dose escalation of SDF-1 were loaded into collagen scaffolds containing BMP, VEGF, or PDGF, and implanted into subcutaneous sites at mouse dorsa or calvarial critical-sized bone defects for 2 and 4 weeks. The harvested biopsies were examined by microCT and histology. The results demonstrated that while SDF-1 had no effect in the ectopic bone model in promoting de novo osteogenesis, however, in the orthotopic bone model of the critical-sized defects, SDF-1 enhanced calvarial critical-sized bone defect healing similar to VEGF, and PDGF. These results suggest that SDF-1 plays a role in the repair of large critical-sized defect where more cells are needed while not impacting de novo bone formation, which may be associated with the functions of SDF-1 on circulating stem cell recruitment and angiogenesis." @default.
• W1986543403 created "2016-06-24" @default.
• W1986543403 creator A5044774272 @default.
• W1986543403 creator A5046679612 @default.
• W1986543403 date "2014-05-06" @default.
• W1986543403 modified "2023-09-23" @default.
• W1986543403 title "SDF-1 Enhances Wound Healing of Critical-Sized Calvarial Defects beyond Self-Repair Capacity" @default.
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• W1986543403 doi "https://doi.org/10.1371/journal.pone.0097035" @default.
• W1986543403 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4011888" @default.
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• W1986543403 hasPublicationYear "2014" @default.
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