title: Delayed fracture healing in tetranectin-deficient mice.
abstract: Tetranectin is a plasminogen-binding protein that enhances plasminogen activation, which has been suggested to play a role in tissue remodeling. Recently, we showed that tetranectin has a role in the wound-healing process. In this study, we investigated whether tetranectin plays a role in fracture healing. The fracture-healing process was studied using a femoral osteotomy model in tetranectin-null mice, previously generated by the authors. Radiographic imaging, micro-computed tomography (μCT), and histological analysis were used to evaluate osteotomy healing. In wild-type mice, a callus was apparent from 7 days, and most samples showed marked callus formation and rebridging of the cortices at the osteotomy site at 21 days. In contrast, in the tetranectin-null mice there was no callus formation at 7 days and much less callus formation and no bridging of cortices were observed at 21 days. At 35 days, all osteotomy sites showed clear rebridging, and secondary bone formation was achieved in wild-type mice by 42 days. In contrast, no clear rebridging or secondary bone formation was observed at 42 days in the tetranectin-null mice. Analysis using μCT at 21 days after osteotomy revealed that the callus area in tetranectin-null mice was smaller than that in wild-type mice. Histological analysis also showed that soft tissue and callus formation were smaller in the tetranectin-null mice at the early stage of the healing process after drill-hole injury. These results suggested that tetranectin could have a role in the positive regulation at the early stage of the fracture-healing process, which was reflected in the delayed fracture healing in tetranectin-deficient mice.
authors.affiliation: Department of Orthopaedic Surgery, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. iba@sapmed.ac.jp
authors.forename: Kousuke
authors.initials: K
authors.lastname: Iba
authors.forename: Yasuhisa
authors.initials: Y
authors.lastname: Abe
authors.forename: Takako
authors.initials: T
authors.lastname: Chikenji
authors.forename: Kumiko
authors.initials: K
authors.lastname: Kanaya
authors.forename: Hironori
authors.initials: H
authors.lastname: Chiba
authors.forename: Koichi
authors.initials: K
authors.lastname: Sasaki
authors.forename: Takayuki
authors.initials: T
authors.lastname: Dohke
authors.forename: Takuro
authors.initials: T
authors.lastname: Wada
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Yamashita
mesh_terms: D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001854:Bone Marrow Cells / Q000201:enzymology / Q000473:pathology; D002454:Cell Differentiation; D002478:Cells, Cultured; D003114:Colony-Forming Units Assay; D005269:Femur / Q000000981:diagnostic imaging / Q000473:pathology*; D017102:Fracture Healing; D037181:Lectins, C-Type / Q000172:deficiency* / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010027:Osteotomy; D017154:Stromal Cells / Q000473:pathology; D013977:Tibia / Q000000981:diagnostic imaging / Q000473:pathology; D055114:X-Ray Microtomography
chemical_list: D015415:Biomarkers; D037181:Lectins, C-Type; C048648:tetranectin; D000469:Alkaline Phosphatase