Suzuki F
Department of Biochemistry, Faculty of Dentistry, Osaka University, Japan.
Connect Tissue Res. 1996;35(1-4):303-7. doi: 10.3109/03008209609029204.
Insulin induces early chondrogenesis in cultures of a clonal cell-line, ATDC5, which was derived from mouse embryonal carcinoma line AT805. Cartilage-generated matrix components chondromodulin-I (ChM-I) synergistically stimulates growth and differentiation of chondrocytes in the presence or absence of FGF-2. In contrast, ChM-I inhibits the proliferation of vascular endothelial cells and tube formation, thereby further stimulating cartilage growth and inhibiting replacing cartilage by bone in an early stage. Another cartilage-derived chondromodulin-II (ChM-II) also stimulates cartilage growth. However, ChM-II does not inhibit vascularization but stimulates osteoclast differentiation. Therefore, endochondral bone formation is regulated sequentially by cartilage-derived multiple autocrine factors. This opens a new mechanism of regulation of endochondral bone formation.
胰岛素可在克隆细胞系ATDC5的培养物中诱导早期软骨形成，该细胞系源自小鼠胚胎癌细胞系AT805。软骨生成的基质成分软骨调节素-I（ChM-I）在有或没有FGF-2的情况下，均可协同刺激软骨细胞的生长和分化。相反，ChM-I抑制血管内皮细胞的增殖和管形成，从而在早期进一步刺激软骨生长并抑制软骨被骨替代。另一种源自软骨的软骨调节素-II（ChM-II）也刺激软骨生长。然而，ChM-II并不抑制血管生成，而是刺激破骨细胞分化。因此，软骨内骨形成由软骨衍生的多种自分泌因子依次调节。这开启了软骨内骨形成调节的新机制。
