Applying vibration in early postmenopausal osteoporosis promotes osteogenic differentiation of bone marrow-derived mesenchymal stem cells and suppresses postmenopausal osteoporosis progression

Biosci Rep. 2019 Sep 3;39(9):BSR20191011. doi: 10.1042/BSR20191011. Print 2019 Sep 30.

Abstract

We aimed to evaluate whether applying low magnitude vibration (LMV) in early postmenopausal osteoporosis (PMO) suppresses its progression, and to investigate underlying mechanisms. Rats were randomly divided into Sham (Sham-operated), Sham+V, OVX (ovariectomized), OVX+E2 (estradiol benzoate), OVX+V (LMV at 12-20 weeks postoperatively), and OVX+Vi (LMV at 1-20 weeks postoperatively) groups. LMV was applied for 20 min once daily for 5 days weekly. V rats were loaded with LMV at 12-20 weeks postoperatively. Vi rats were loaded with LMV at 1-20 weeks postoperatively. Estradiol (E2) rats were intramuscularly injected at 12-20 weeks postoperatively once daily for 3 days. The bone mineral densities (BMDs), biomechanical properties, and histomorphological parameters of tibiae were analyzed. In vitro, rat bone marrow-derived mesenchymal stem cells (rBMSCs) were subjected to LMV for 30 min daily for 5 days, or 17β-E2 with or without 1-day pretreatment of estrogen receptor (ER) inhibitor ICI 182,780 (ICI). The mRNA and protein expresion were performed. Data showed that LMV increased BMD, bone strength, and bone mass of rats, and the effects of Vi were stronger than those of E2. In vitro, LMV up-regulated the mRNA and protein expressions of Runx2, Osx, Col I, and OCN and down-regulated PPARγ, compared with E2. The effects of both LMV and E2 on rBMSCs were inhibited by ICI. Altogether, LMV in early PMO suppresses its progression, which is associated with osteogenic differentiation of rBMSCs via up-regulation of ERα and activation of the canonical Wnt pathway. LMV may therefore be superior to E2 for the suppression of PMO progression.

Keywords: ERα; Wnt; low magnitude vibration; postmenopausal osteoporosis; rat bone marrow-derived mesenchymal stem cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Density / drug effects
  • Bone Density / genetics
  • Bone Marrow Cells / cytology
  • Bone Marrow Cells / drug effects
  • Bone Marrow Cells / metabolism
  • Cell Differentiation / drug effects
  • Collagen Type I / genetics
  • Collagen Type I / metabolism
  • Core Binding Factor Alpha 1 Subunit / genetics
  • Core Binding Factor Alpha 1 Subunit / metabolism
  • Disease Models, Animal
  • Disease Progression
  • Estradiol / analogs & derivatives
  • Estradiol / pharmacology
  • Estrogen Receptor Antagonists / pharmacology
  • Estrogen Receptor alpha / genetics
  • Estrogen Receptor alpha / metabolism
  • Female
  • Fulvestrant / pharmacology
  • Gene Expression Regulation*
  • Humans
  • Mesenchymal Stem Cells / cytology
  • Mesenchymal Stem Cells / drug effects
  • Mesenchymal Stem Cells / metabolism*
  • Osteocalcin / genetics
  • Osteocalcin / metabolism
  • Osteogenesis / drug effects
  • Osteogenesis / genetics*
  • Osteoporosis, Postmenopausal / genetics
  • Osteoporosis, Postmenopausal / pathology
  • Osteoporosis, Postmenopausal / surgery
  • Osteoporosis, Postmenopausal / therapy*
  • Ovariectomy
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction
  • Tibia / drug effects
  • Tibia / metabolism
  • Tibia / pathology
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Vibration / therapeutic use*

Substances

  • Collagen Type I
  • Core Binding Factor Alpha 1 Subunit
  • Estrogen Receptor Antagonists
  • Estrogen Receptor alpha
  • PPAR gamma
  • Runx2 protein, rat
  • Sp7 protein, rat
  • Transcription Factors
  • Osteocalcin
  • estradiol 3-benzoate
  • Fulvestrant
  • Estradiol