First Author | Wang M | Year | 2011 |
Journal | Osteoarthritis Cartilage | Volume | 19 |
Issue | 6 | Pages | 751-62 |
PubMed ID | 21420501 | Mgi Jnum | J:172689 |
Mgi Id | MGI:5008537 | Doi | 10.1016/j.joca.2011.03.004 |
Citation | Wang M, et al. (2011) Smad1 plays an essential role in bone development and postnatal bone formation. Osteoarthritis Cartilage 19(6):751-62 |
abstractText | OBJECTIVES: To determine the role of Smad1 in bone development and postnatal bone formation. METHODS: Col2a1-Cre transgenic mice were bred with Smad1(fx/fx) mice to produce chondrocyte-specific Smad1 conditional knockout (cKO) mice. Embryonic skeletal preparation and staining were performed, alkaline phosphatase activity (ALP) and relative gene expression were examined in isolated primary cells. Smad1(fx/fx) mice were also bred with Col1a1-Cre transgenic mice to produce osteoblast-specific Smad1 cKO mice. Postnatal bone formation was assessed by micro-computed tomography (muCT) and histological analyses in 2-month-old mice. Mineralized bone nodule formation assay, 5-bromo-2'-deoxy-uridine (BrdU) labeling and gene expression analysis were performed. RESULTS: Mice with chondrocyte- and osteoblast-specific deletion of the Smad1 gene are viable and fertile. Calvarial bone development was delayed in chondrocyte-specific Smad1 cKO mice. In osteoblast-specific Smad1 cKO mice, BMP signaling was partially inhibited and mice developed an osteopenic phenotype. Osteoblast proliferation and differentiation were impaired in osteoblast-specific Smad1 cKO mice. CONCLUSIONS: Smad1 plays an essential role in bone development and postnatal bone formation. |