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Compressive force-produced CCN2 induces osteocyte apoptosis through ERK1/2 pathway.

Kenji Hoshi1, Harumi Kawaki, Ichiro Takahashi

  • 1Division of Orthodontics and Dentofacial Orthopedics, Tohoku University Graduate School of Dentistry, Sendai, Japan.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|October 25, 2013
PubMed
Summary

Mechanical force triggers CCN2 production in osteocytes, leading to cell death via the ERK1/2 pathway. This study reveals CCN2

Keywords:
APOPTOSISCCN2ERK1/2MECHANICAL STRESSOSTEOCYTE

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Area of Science:

  • Bone Biology
  • Cellular Mechanotransduction
  • Osteocyte Function

Background:

  • Osteocytes are crucial for bone remodeling and homeostasis, responding to mechanical stimuli.
  • CCN2 (Cellular Communication Network factor 2) is implicated in bone biology, but its specific role in osteocytes remains unclear.

Purpose of the Study:

  • To investigate the function of CCN2 in osteocytes under mechanical stress.
  • To elucidate the molecular mechanisms by which CCN2 affects osteocytes subjected to compressive force.

Main Methods:

  • Compressive force loading on osteocytes.
  • Measurement of CCN2 gene expression and protein production.
  • Induction of apoptosis using exogenous CCN2 and assessment via neutralizing antibodies.
  • Analysis of extracellular signal-regulated kinase 1/2 (ERK1/2) pathway activation using inhibitors.

Main Results:

  • Compressive force significantly increased CCN2 gene expression and production in osteocytes.
  • CCN2 induced apoptosis in osteocytes, which was blocked by a CCN2-neutralizing antibody.
  • Loading-induced osteocyte apoptosis was mediated by the activation of the ERK1/2 pathway.
  • Exogenous CCN2 activated ERK1/2, and blocking CCN2 inhibited loading-induced ERK1/2 activation.

Conclusions:

  • Enhanced CCN2 production in osteocytes under compressive force induces apoptosis.
  • The apoptosis-inducing effect of CCN2 is mediated through the activation of the ERK1/2 signaling pathway.
  • This study identifies a novel mechanism of osteocyte mechanotransduction involving CCN2 and ERK1/2.