IL-1beta induces and TGF-beta reduces vitamin D3-induced bone resorption in mouse calvarial bone cells.

Bone cells produce multiple growth factors and cytokines that have effects on bone metabolism and can be incorporated into the bone matrix. The present study was designed to extend these observations by examining the interactions between transforming growth factor-beta (TGF-beta) or interleukin-1beta (IL-1beta) and bone cells in a rat long bone culture model. IL-1beta regulates several activities of the osteoblast cells derived from rat long bone explants in vitro. IL-1beta stimulated cellular proliferation and the synthesis of prostaglandin E2 and plasminogen activator activity in the cultured cells in a dose-dependent manner. TGF-B is present in the bone matrix and potentially can be released during bone resorption. TGF-beta reduced basal bone resorption and inhibited vitamin D3 [1,25(OH)2D3]-induced bone resorption in rat long bone cells. These studies support the role of IL-1beta in the pathological modulation of bone cell metabolism, with regard to implication in the pathogenesis of osteoporosis by IL-1beta, and that TGF-beta is positively inhibiting the bone resorption.