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Glucocorticoid receptor and sequential P53 activation by dexamethasone mediates apoptosis and cell cycle arrest of

Hui Li1, Wenwei Qian, Xisheng Weng

  • 1Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.

Plos One
|June 22, 2012
PubMed

Insights

Dexamethasone inhibits osteoblast proliferation by inducing apoptosis and cell cycle arrest. This process is mediated by the glucocorticoid receptor (GR) and p53 activation, impacting bone cell growth.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Endocrinology

Background:

  • Glucocorticoids are crucial for osteoblast proliferation.
  • The precise molecular mechanisms remain unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms behind dexamethasone's inhibitory effects on murine osteoblastic MC3T3-E1 cells.
  • To elucidate the roles of glucocorticoid receptor (GR) and p53 in this process.

Main Methods:

  • Cell culture of MC3T3-E1 cells.
  • Treatment with dexamethasone, GR blocker RU486, and p53 RNA interference.
  • Analysis of cell cycle, apoptosis, and gene expression (p21, NOXA, PUMA).

Main Results:

  • Dexamethasone induced apoptosis and G1 phase arrest in MC3T3-E1 cells.
  • These effects were dependent on glucocorticoid receptor (GR) activation.
  • Apoptosis and cell cycle arrest were mediated by p53-dependent upregulation of p21, NOXA, and PUMA.

Conclusions:

  • Dexamethasone directly inhibits osteoblast proliferation via GR and p53 activation.
  • Aberrant GR and subsequent p53 activation lead to cell cycle arrest and apoptosis in osteoblasts.

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