Modulation of Matrix Mineralization by von Willebrand Factor C Domain Containing 2 in Vivo and in Vitro

DOI Open Access
  • KANEMARU Tomoki
    Department of Maxillofacial Surgery, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan
  • OHYAMA Yoshio
    Department of Maxillofacial Surgery, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan Department of Oral and Maxillofacial Surgery, Shizuoka city Shizuoka Hospital, Shizuoka, Japan
  • AOKI Kazuhiro
    Department of Basic Oral Health Engineering, Graduate School of Medical and Dental Sciences,
  • TAMURA Atsushi
    Department of Organic Biomaterials, Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University, Tokyo, Japan
  • YUI Nobuhiko
    Department of Organic Biomaterials, Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University, Tokyo, Japan
  • YAMAGUCHI Satoshi
    Department of Maxillofacial Surgery, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan
  • MOCHIDA Yoshiyuki
    Department of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America

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Abstract

<p>Cysteine knot proteins (CKPs) with cysteine-rich domain mainly inhibit bone formation induced by Bone morphogenetic protein (BMP). We identified a novel CKP, von Willebrand factor C domain containing 2 (VWC2), and investigated the effect of VWC2 on bone formation. When VWC2 was added to MC3T3-E1 osteoblastic cell culture, the extent of matrix mineralization and alkaline phosphatase activity were significantly increased. The newly formed bone area was increased and mineral apposition rate was enhanced by VWC2 when applied to mouse cranial bone defect in vivo. VWC2 addition also increased the expression of key osteogenic markers Osterix and Runt-related transcription factor 2 (Runx2) in primary osteoblast cells. In conclusion, VWC2 positively regulates bone formation possibly through Osterix and Runx2 upregulation.</p>

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