The Stimulatory Effect of Dexamethasone on RANKL-induced Osteoclastogenesis

Dexamethasone에 의한 RANKL 유도성 파골세포 분화 촉진 효과

  • No, A-Long-Sae-Mi (College of Pharmacy, Sookmyung Women's University) ;
  • Chen, Ling (College of Pharmacy, Sookmyung Women's University) ;
  • Park, Hyo-Jung (College of Pharmacy, Sookmyung Women's University) ;
  • Yang, Mi-Hye (College of Natural Sciences, Kyungpook National University) ;
  • Lee, Jung-Min (College of Pharmacy, Sookmyung Women's University) ;
  • Yim, Mi-Jung (College of Pharmacy, Sookmyung Women's University)
  • 노아롱새미 (숙명여자대학교 약학대학) ;
  • 천링 (숙명여자대학교 약학대학) ;
  • 박효정 (숙명여자대학교 약학대학) ;
  • 양미혜 (경북대학교 자연과학대학 생명공학부) ;
  • 이정민 (숙명여자대학교 약학대학) ;
  • 임미정 (숙명여자대학교 약학대학)
  • Published : 2009.04.30

Abstract

We explored the effects of dexamethasone on osteoclast precursors using BMMs. Dexamethasone inhibited the proliferation of BMMs. Furthermore, it stimulated the osteoclast formation via NFATc1 activation in the presence of RANKL. Since dexamethasone targeted the early stage of osteoclast formation, we investigated its effect on mRNA expression of GR and $IFN-{\beta}$. Whereas dexamethasone had no effects on GR expression in the presence of RANKL, it reduced the expression of $IFN-{\beta}$, suggesting that dexamethasone increased RANKL-induced osteoclast formation by modulating $IFN-{\beta}$.

Keywords

References

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