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Related Experiment Videos

Mechanical strain activates estrogen response elements in bone cells.

G Zaman1, M Z Cheng, H L Jessop

  • 1Department of Veterinary Basic Sciences, The Royal Veterinary College, London, UK. gzaman@rvc.ac.uk

Bone
|July 29, 2000
PubMed
Summary
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Mechanical strain and estrogen both stimulate bone cell proliferation by activating estrogen receptors (ER alpha). This effect, mediated by estrogen-responsive genes, is blocked by estrogen antagonists, highlighting ER alpha

Area of Science:

  • Cell Biology
  • Endocrinology
  • Biomechanical Engineering

Background:

  • Estrogen plays a crucial role in bone health and remodeling.
  • Mechanical strain is a known stimulus for bone formation.
  • The specific role of the estrogen receptor in mediating cellular responses to mechanical strain in bone cells requires further elucidation.

Purpose of the Study:

  • To investigate the involvement of the estrogen receptor (ER alpha) in the early cellular responses of bone cells to mechanical strain.
  • To compare the effects of mechanical strain and 17 beta-estradiol on cell proliferation and estrogen-responsive gene activity.
  • To determine if the estrogen antagonist ICI 182,780 can block strain-induced responses in bone cells.

Main Methods:

  • Subconfluent monolayer cultures of ROS.SMER #14 cells (osteoblasts overexpressing ER alpha) and ROS 17/2.8 cells were subjected to dynamic mechanical strain or treated with 17 beta-estradiol.

Related Experiment Videos

  • Cell proliferation rates were measured.
  • Estrogen-responsive reporter gene activity (ERE-CAT) was assessed following transient transfection with 2ERE-pS2-CAT.

    • Main Results:

    • Mechanical strain and 17 beta-estradiol significantly increased proliferation in ROS.SMER #14 cells compared to ROS 17/2.8 cells.
    • Strain and estradiol treatment led to increased estrogen-responsive element (ERE) activity, with greater effects observed in cells with higher ER alpha expression.
    • The estrogen antagonist ICI 182,780 effectively blocked both strain- and estradiol-induced increases in proliferation and ERE activity.

    Conclusions:

    • Mechanical strain, similar to estrogen, stimulates proliferation in osteoblast-like cells.
    • These strain-induced cellular responses involve the activation of ER alpha and estrogen-responsive genes.
    • The findings indicate that ER alpha plays a significant role in mediating the early cellular responses of bone cells to mechanical stimuli.