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A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
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Dicer ablation in osteoblasts by Runx2 driven cre-loxP recombination affects bone integrity, but not

Peng Liu1,2, Mario Baumgart2, Marco Groth2

  • 1Institute of Comparative Molecular Endocrinology (CME), Ulm University, Ulm, Germany.

Scientific Reports
|August 25, 2016
PubMed

Insights

Glucocorticoid-induced osteoporosis (GIO) involves microRNAs. Dicer-dependent microRNAs in bone cells play a minor role in GIO, as their absence did not alter the negative effects of glucocorticoids on bone formation.

Area of Science:

  • Molecular Biology
  • Endocrinology
  • Bone Biology

Background:

  • Glucocorticoid-induced osteoporosis (GIO) is a significant adverse effect of long-term glucocorticoid (GC) treatment.
  • GIO primarily occurs through suppressed bone formation and osteoblast differentiation, independent of GC receptor (GR) dimerization.
  • MicroRNAs are crucial regulators of osteoblast differentiation.

Purpose of the Study:

  • To investigate the role of Dicer-dependent microRNAs in GC-induced suppression of osteoblast differentiation.
  • To elucidate the GR dimer-dependent and -independent microRNA expression patterns under GC treatment.
  • To determine the functional significance of microRNAs in GIO pathogenesis.

Main Methods:

  • MicroRNA sequencing on dexamethasone-treated wild-type and GR dimer-deficient mesenchymal stromal cells.
  • Generation of mice with osteoblast-specific deletion of Dicer (Dicer(Runx2Cre)).
  • In vitro analysis of Dicer-deficient osteoblasts (proliferation, differentiation, mineralization) and in vivo GIO models.

Main Results:

  • GC treatment altered miRNA expression in a GR dimer-dependent and -independent manner.
  • Osteoblast-specific Dicer deletion resulted in growth retardation and impaired bone formation.
  • However, GIO induction showed similar bone formation reduction in Dicer(Runx2Cre) mice and controls.
  • GC treatment suppressed differentiation of Dicer-deficient osteoblasts to the same extent as wild-type cells.

Conclusions:

  • Dicer-dependent small RNA biogenesis in osteoblasts plays a minor role in the pathogenesis of GC-induced bone formation inhibition.
  • GC-induced suppression of osteoblast differentiation is largely independent of Dicer-dependent microRNAs.

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