Interleukin-$1{\beta}$ induces bone resorption by regulation of prostaglandin $E_2$ synthesis and plasminogen activator activity, and TGF-$\beta$ inhibits bone resorption of rat bone cells

쥐의 골세포에서 $PGE_2$ 합성과 plasminogen activator 활성 조절에 의한 IL-$1{\beta}$의 골 흡수유도와 TGF-$\beta$에 의한 골 흡수 억제 기전에 관한 연구

  • 김영훈 (경희대학교 치과대학 교정학교실) ;
  • 이영준 (경희대학교 치과대학 교정학교실) ;
  • 정규림 (경희대학교 치과대학 교정학교실) ;
  • 박영국 (경희대학교 치과대학 교정학교실)
  • Published : 2000.12.01

Abstract

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-$1\beta$(rhIL-$1\beta$) and bone cells in a rat long bone culture model. IL-$1\beta$ regulates several activities of the osteoblast cells derived from rat long bone explants in vitro. IL-$1\beta$ stimulated cellular proliferation as well as the synthesis of prostaglandin $E_2$ 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 $D_3[1,25(OH)_2D_3]$-induced bone resorption in rat long bone cells. These results support the role of IL-$1\beta$ in the pathological modulation of bone cell metabolism, with regard to implication in the Pathogenesis of osteoporosis by IL-$1\beta$, and that TGF-$\beta$ positively inhibits the bone resorption.