title: Stromal cell-derived factor-1 enhances distraction osteogenesis-mediated skeletal tissue regeneration through the recruitment of endothelial precursors.
abstract: Distraction osteogenesis (DO) is a unique therapy that induces skeletal tissue regeneration without stem/progenitor cell transplantation. Although the self-regeneration property of DO provides many clinical benefits, the long treatment period required is a major drawback. A high-speed DO mouse model (H-DO), in which the distraction was done two times faster than in control DO (C-DO) mice, failed to generate new bone callus in the DO gap. We found that this was caused by the unsuccessful recruitment of bone marrow endothelial cells (BM-ECs)/endothelial progenitor cells (EPCs) into the gap. We then tested the ability of a local application of stromal cell-derived factor-1 (SDF-1), a major chemo-attractant for BM-ECs/EPCs, to accelerate the bone regeneration in H-DO. Our data showed that, in H-DO, SDF-1 induced callus formation in the gap through the recruitment of BM-ECs/EPCs, the maturation of neo-blood vessels, and increased blood flow. These results indicate that the active recruitment of endogenous BM-ECs/EPCs may provide a substantial clinical benefit for shortening the treatment period of DO.
authors: Department of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
authors: Masahito
authors: M
authors: Fujio
authors: Akihito
authors: A
authors: Yamamoto
authors: Yuji
authors: Y
authors: Ando
authors: Ryutaro
authors: R
authors: Shohara
authors: Kazuhiko
authors: K
authors: Kinoshita
authors: Tadashi
authors: T
authors: Kaneko
authors: Hideharu
authors: H
authors: Hibi
authors: Minoru
authors: M
authors: Ueda
mesh_terms: D000818:Animals; D001808:Blood Vessels / Q000378:metabolism / Q000473:pathology; D001854:Bone Marrow Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D001861:Bone Regeneration / Q000187:drug effects; D001842:Bone and Bones / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D002146:Bony Callus / Q000187:drug effects / Q000473:pathology; D054377:Chemokine CXCL12 / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D042783:Endothelial Cells / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D005260:Female; D006801:Humans; D007511:Ischemia / Q000473:pathology; D051379:Mice; D008813:Mice, Inbred ICR; D023421:Models, Animal; D018919:Neovascularization, Physiologic / Q000187:drug effects; D019857:Osteogenesis, Distraction; D054387:Receptors, CXCR / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000378:metabolism; D013234:Stem Cells / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects
chemical_list: C514936:CXCR4 protein, mouse; D054377:Chemokine CXCL12; C501897:Cmkor1 protein, mouse; D054387:Receptors, CXCR; D019718:Receptors, CXCR4