Title : Stimulation of osteoclast formation by RANKL requires interferon regulatory factor-4 and is inhibited by simvastatin in a mouse model of bone loss.

Pub. Date : 2013

PMID : 24039733






5 Functional Relationships(s)
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1 Stimulation of osteoclast formation by RANKL requires interferon regulatory factor-4 and is inhibited by simvastatin in a mouse model of bone loss. Simvastatin tumor necrosis factor (ligand) superfamily, member 11 Mus musculus
2 We found that in vitro, IRF4 expression is upregulated during osteoclast differentiation induced by RANKL (receptor activator of nuclear factor-kappaB ligand), while simvastatin blocks RANKL-induced osteoclastogenesis and decreases expression of NFATc1 (nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1), IRF4 and osteoclast markers. Simvastatin tumor necrosis factor (ligand) superfamily, member 11 Mus musculus
3 To investigate the in vivo effects of simvastatin in RANKL-treated mice, we examined the bone mineral density (BMD) of a mouse model of bone loss, and found that simvastatin significantly reduced bone loss by suppressing osteoclast numbers in vivo, even in the presence of high concentrations of RANKL. Simvastatin tumor necrosis factor (ligand) superfamily, member 11 Mus musculus
4 To investigate the in vivo effects of simvastatin in RANKL-treated mice, we examined the bone mineral density (BMD) of a mouse model of bone loss, and found that simvastatin significantly reduced bone loss by suppressing osteoclast numbers in vivo, even in the presence of high concentrations of RANKL. Simvastatin tumor necrosis factor (ligand) superfamily, member 11 Mus musculus
5 The results are consistent with the hypothesis that simvastatin blocks RANKL-induced IRF4 expression in osteoclastogenesis. Simvastatin tumor necrosis factor (ligand) superfamily, member 11 Mus musculus