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A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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MicroRNA-17/20a inhibits glucocorticoid-induced osteoclast differentiation and function through targeting RANKL

Changgui Shi1, Jin Qi2, Ping Huang2

  • 1Department of Orthopedics, Changzheng Hospital, Second Military Medical University of China, Shanghai, China.

Bone
|August 21, 2014
PubMed

Insights

Glucocorticoids increase bone loss by up-regulating RANKL in osteoblasts. MicroRNA-17/20a counteracts this by targeting RANKL, suggesting a therapeutic target for glucocorticoid-induced bone resorption.

Area of Science:

  • Molecular Biology
  • Endocrinology
  • Bone Biology

Background:

  • Glucocorticoids induce bone loss by promoting osteoclast differentiation and bone resorption.
  • The precise molecular mechanisms underlying glucocorticoid-induced osteoclastogenesis are not fully elucidated.
  • Glucocorticoids are known to decrease microRNA-17-92a cluster expression in osteoblasts.

Purpose of the Study:

  • To investigate the role of microRNA-17/20a in regulating Receptor Activator of Nuclear Factor kappa-B Ligand (RANKL) expression in osteoblasts.
  • To determine if microRNA-17/20a mediates the effects of glucocorticoids on osteoclast differentiation and function.

Main Methods:

  • Western blot analysis to assess RANKL protein levels.
  • Luciferase reporter assay to confirm post-transcriptional regulation of RANKL by microRNA-17/20a.
  • Co-culture experiments with osteoblasts overexpressing microRNA-17/20a and osteoclast progenitors.

Main Results:

  • MicroRNA-17/20a significantly reduced RANKL protein levels and attenuated dexamethasone-induced RANKL expression in osteoblasts.
  • Post-transcriptional repression of RANKL by microRNA-17/20a was confirmed.
  • Dexamethasone-induced osteoclast differentiation and function were significantly inhibited in co-cultures with osteoblasts overexpressing microRNA-17/20a.

Conclusions:

  • MicroRNA-17/20a directly targets RANKL mRNA in osteoblasts, inhibiting its expression.
  • Down-regulation of microRNA-17/20a by glucocorticoids contributes to increased RANKL expression, promoting osteoclastogenesis.
  • MicroRNA-17/20a plays a crucial role in modulating glucocorticoid effects on osteoclast differentiation and function, presenting a potential therapeutic target.
Keywords:
GlucocorticoidsOsteoclastsOsteoporosisRANKLmicroRNA-17/20a

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