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MicroRNA-338-3p inhibits glucocorticoid-induced osteoclast formation through RANKL targeting

X H Zhang1, G L Geng2, B Su3

  • 1Department of Physical Therapy, Wuxi Tongren International Rehabilitation Hospital, Wuxi, Jiangsu, China.

Genetics and Molecular Research : GMR
|October 6, 2016
PubMed

Insights

MicroRNA-338-3p (miR-338-3p) inhibits glucocorticoid-induced osteoclast formation. This microRNA targets RANKL, suggesting a role in osteoporosis by regulating osteoclast differentiation and bone resorption.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Osteoporosis is linked to impaired osteoclast precursor (pre-OC) differentiation.
  • MicroRNAs (miRNAs) are critical regulators of pre-OC differentiation and are implicated in osteoporosis research.
  • Glucocorticoids (GCs) influence bone metabolism, and their associated miRNAs are of recent interest.

Purpose of the Study:

  • To investigate the expression and function of glucocorticoid-associated microRNA-338-3p (miR-338-3p) in osteoclast formation.
  • To elucidate the role of miR-338-3p in glucocorticoid-induced osteoclast differentiation and bone resorption.

Main Methods:

  • Analyzing miR-338-3p expression in response to dexamethasone (a GC) in pre-OCs.
  • Using miR-338-3p mimics and inhibitors to assess effects on osteoclast differentiation and bone resorption.
  • Investigating the regulatory relationship between miR-338-3p and RANKL (receptor activator of nuclear factor kappa-B ligand).
  • Confirming RANKL as a direct target of miR-338-3p and assessing rescue experiments.

Main Results:

  • Dexamethasone treatment inhibited miR-338-3p expression and promoted osteoclast differentiation.
  • Overexpression of miR-338-3p attenuated GC-induced osteoclast formation and bone resorption.
  • Inhibition of miR-338-3p reversed these effects.
  • RANKL expression was inversely correlated with miR-338-3p levels and was identified as a direct target.
  • Re-introducing RANKL reversed the inhibitory effects of miR-338-3p.

Conclusions:

  • miR-338-3p plays a significant role in regulating glucocorticoid-induced osteoclast differentiation and function.
  • The mechanism involves miR-338-3p targeting RANKL, thereby modulating osteoclast activity.
  • These findings offer insights into potential therapeutic strategies for osteoporosis related to GC use.

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