beta ig-h3 is a TGF-beta-induced extracellular matrix protein which is expressed in many tissues including bones and cartilages. In previous reports, we showed that beta ig-h3 mediates cell adhesion and migration and, especially in bones, negatively regulates the mineralization in the end stage of endochondral ossification. Here, to elucidate the expression pattern and role of beta ig-h3 in chondrocyte differentiation, ATDC5 chondrocytes and embryonic and postnatal mice were used for in vitro differentiation studies and in vivo studies, respectively. beta ig-h3 was strongly induced by the treatment of TGF-beta1 and the expression level of beta ig-h3 mRNA and protein were highly expressed in the early stages of differentiation but decreased in the late stages in ATDC5. Furthermore, the patterns of TGF-beta1, -beta2, and -beta3 mRNA expression were concurrent with beta ig-h3 in ATDC5. beta ig-h3 was deeply stained in perichondrium (PC), periosteum (PO), and prehypertrophic chondrocytes (PH) through the entire period of endochondral ossification in mice. beta ig-h3 was mainly expressed in PC and PH at embryonic days and obviously in PH in postnatal days. These results suggest that beta ig-h3 may play a critical role as a regulator of chondrogenic differentiation in endochondral ossification.
Animals ; Cell Differentiation/genetics ; Chondrocytes/*metabolism ; Chondrogenesis/*genetics ; Embryo, Mammalian ; Extracellular Matrix Proteins/*genetics/metabolism ; Femur/embryology/growth & development/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Mice ; Mice, Inbred ICR ; Osteogenesis/*genetics ; Transforming Growth Factor beta/*genetics/metabolism ; Tumor Cells, Cultured