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

Tomoki KANEMARU; Yoshio OHYAMA; Kazuhiro AOKI; Atsushi TAMURA; Nobuhiko YUI; Satoshi YAMAGUCHI; Yoshiyuki MOCHIDA

doi:10.11223/jarde.15.131

ORIGINAL ARTICLES

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

Tomoki KANEMARU, Yoshio OHYAMA, Kazuhiro AOKI, Atsushi TAMURA, Nobuhiko YUI, Satoshi YAMAGUCHI, Yoshiyuki MOCHIDA

Author information

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

Keywords: : VWC2, CKPs, growth factor, matrix mineralization, bone formation

JOURNAL FREE ACCESS

2018 Volume 15 Issue 3 Pages 131-142

DOI https://doi.org/10.11223/jarde.15.131

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Abstract

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.

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