Korean J Orthod.
2000 Dec;30(6):713-721.
Interleuken-1beta induces bone resorption by regulation of prostaglandin E2 synthesis and plasminogen activator activity, and TGF-beta inhibits bone resorption of rat bone cells
- Affiliations
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- 1Department of Orthodontics, Kyung Hee University, Korea. ygpark@khu.ac.kr
Abstract
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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 (rhIL-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 as well as the synthesis of prostaglandin E2 and plasminogen activator activity in the cultured cells in a dose-dependent manner. TGF-beta is present in the bone matrix and potentially 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 results 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 positively inhibits the bone resorption.