Horm Metab Res 2005; 37(10): 589-592
DOI: 10.1055/s-2005-870538
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Statins Modulate the Levels of Osteoprotegerin/Receptor Activator of NFκB Ligand mRNA in Mouse Bone-cell Cultures

H.  Kaji1 , M.  Kanatani1 , T.  Sugimoto2 , K.  Chihara1
  • 1Division of Endocrinology/Metabolism, Neurology and Hematology/Oncology, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan
  • 2Division of Endocrinology/Metabolism and Hematological Oncology, Shimane University School of Medicine, 89-1, Enya-cho, Izumo, Shimane, 693-8501, Japan
Further Information

Publication History

Received 29 November 2004

Accepted after second revision 18 May 2005

Publication Date:
08 November 2005 (online)

Abstract

Statins stimulate bone formation partly by inducing osteoblast differentiation, although there is controversy about the effects of statins on bone mineral density and fracture risk. Several studies have revealed that statins suppress bone resorption. However, the mechanism by which statins inhibit bone resorption is still unclear. The present study was performed to clarify the effects of statins on osteoclast formation as well as the levels of osteoprotegerin (OPG) and receptor activator of NFκB ligand (RANKL) mRNA in mouse bone-cell cultures by semiquantitative RT-PCR. 10 - 8 M 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] significantly stimulated osteoclast formation and 10 - 6 M statins (mevastatin and simvastatin) significantly antagonized osteoclast formation stimulated by 1,25(OH)2D3 in mouse bone-cell cultures, including both osteoblasts and osteoclasts. 10 - 6 M mevastatin and simvastatin increased the level of OPG mRNA in mouse bone-cell cultures. On the other hand, 10 - 6 M mevastatin and simvastatin inhibited the level of RANKL mRNA in these cultures. In conclusion, the present study demonstrates that statins inhibit osteoclast formation in mouse bone-cell cultures. Moreover, statins also increased and decreased the levels of OPG and RANKL mRNA expression in these cultures, respectively. The modulation of OPG/RANKL may be involved in the inhibition of osteoclast formation by statins.

References

Hiroshi Kaji, M. D.

Division of Endocrinology/Metabolism, Neurology and Hematology/Oncology, Department of Clinical Molecular Medicine

Kobe University Graduate School of Medicine · 7-5-1 Kusunoki-cho, Chuo-ku · Kobe 650-0017 · Japan

Phone: +81 78 382 5885 ·

Fax: +81 78 382 5899

Email: hiroshik@med.kobe-u.ac.jp

    >