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KMID : 1007020100080010047
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Korean Soceity of Osteroporosis
2010 Volume.8 No. 1 p.47 ~ p.55
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Differential Expression of RANKL and OPG by the PPAR gamma Agonist Rosiglitazone in Osteoblasts
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Lee Myoung-Joo
Lee Soo-Yeon
Park Sang-Hyeon
Ahn Do-Whan
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Abstract
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Objectives: Osteoblasts secrete receptor activator of nuclear factor-kB ligand (RANKL) and osteoprotegerin (OPG). RANKL stimulates osteoclastogenesis but OPG inhibits it by binding with RANKL. Although peroxisome proliferation-activated receptor gamma (PPARγ) has a major role in adipocyte differentiation, it is also involved in bone remodeling. The aim of this study was to examine whether rosiglitazone, the PPARγ agonist, regulates the expression of RANKL and OPG in osteoblasts.
Methods: MC3T3-E1 osteoblasts were cultured and treated with different concentrations of rosiglitazone. Cell viability was assayed with MTT. A conventional PCR was used for the detection of PPARγ gene. Expression of RANKL and OPG mRNA and their protein levels was analyzed by quantitative real-time RT- PCR and Western blot, respectively.
Results: PPARγ mRNA was expressed in MC3T3-E1 osteoblasts and its expression was greatly increased by treatment of 5μM rosiglitazone. Treatment with 1 to 10μM rosiglitazone did not affect cell viability. Compared with vehicle, rosiglitazone (5μM) up-regulated OPG mRNA expression by 2.3-fold and down- regulated RANKL mRNA expression by 5-fold, which was reversed by the PPARγ antagonist GW9662. The level of RANKL and OPG protein varied as compared to their mRNA expression.
Conclusion: These results demonstrate that activation of PPARγ by rosiglitazone induces both down- regulation of RANKL and up-regulation of OPG in osteoblasts, which is likely to cause an inhibition of osteoclastogenesis.
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KEYWORD
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OPG, Osteoblast, RANKL, Rosiglitazone
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