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Bone morphogenetic protein rescues the lack of secondary cartilage in Runx2 ‐deficient mice
Author(s) -
Fukuoka Hiroki,
Shibata Shunichi,
Suda Naoto,
Yamashita Yasuo,
Komori Toshihisa
Publication year - 2007
Publication title -
journal of anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 118
eISSN - 1469-7580
pISSN - 0021-8782
DOI - 10.1111/j.1469-7580.2007.00739.x
Subject(s) - runx2 , chondrocyte , cartilage , bone morphogenetic protein 2 , mesenchymal stem cell , microbiology and biotechnology , type ii collagen , bone morphogenetic protein , extracellular matrix , anatomy , periosteum , chemistry , osteoblast , biology , biochemistry , in vitro , gene
Secondary cartilages including mandibular condylar cartilage have unique characteristics. They originate from alkaline phosphatase (ALP)‐positive progenitor cells of the periosteum, and exhibit characteristic modes of differentiation. They also have a unique extracellular matrix, and coexpress type I, II and X collagens. We have previously shown that there is a total absence of secondary cartilages in Runx2 ‐deficient ( Runx2 –/–) mice. To clarify whether Runx2 is essential for chondrocytic differentiation of secondary cartilages, we performed an organ culture system using mandibular explants derived from Runx2 –/– mice at embryonic day 18.0. Since mRNA for bone morphogenetic protein 2 (BMP2) was strongly expressed in osteoblasts of condylar anlagen in wild‐type mice, and was down‐regulated in those of Runx2 –/– mice, we chose to investigate BMP2 effects on secondary cartilage formation. Condensed mesenchymal cells of mandibular condylar anlagen in precultured explants were ALP‐positive and expressed type I collagen and Sox9 . After culture with recombinant human (rh) BMP2, chondrocytic cells showing ALP activity and expressing Sox5 , Sox9 , and type I and II collagens, appeared from mesenchymal condensation. This expression profile was comparable with the reported pattern of chondrocytes in mouse secondary cartilages. However, chondrocyte hypertrophy was not observed in the explants. These findings indicate that BMP2 partially rescued chondrocyte differentiation but not chondrocyte hypertrophy in secondary cartilage formation in Runx2 –/– mice. Runx2 is required for chondrocyte hypertrophy in secondary cartilage formation, and it is likely that BMP2, which is abundantly secreted by osteoblasts in condylar anlagen, contributes to the early process of secondary cartilage formation.