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06:17
Osteoclast Derivation from Mouse Bone Marrow
Published on: November 6, 2014
Glucocorticoid receptor signaling in bone cells
Paraskevi Moutsatsou1, Eva Kassi, Athanasios G Papavassiliou
1Department of Biological Chemistry, University of Athens Medical School, 75, Mikras Asias Street, 11527 Athens, Greece.
Trends in Molecular Medicine
|May 15, 2012
Summary
Glucocorticoids treat inflammation but cause osteoporosis by affecting bone cells. Understanding glucocorticoid receptor (GR) signaling could lead to selective GR agonists (SEGRAs) that minimize bone loss.
Area of Science:
- Bone Biology
- Endocrinology
- Pharmacology
Background:
- Glucocorticoids are widely used for treating inflammatory and autoimmune diseases.
- A major limitation is their adverse effect on bone metabolism, leading to osteoporosis.
- The glucocorticoid receptor (GR) mediates both therapeutic and adverse effects.
Purpose of the Study:
- To review current knowledge on GR-mediated transcriptional regulation in bone cells.
- To explore the potential for developing selective GR agonists (SEGRAs).
- To dissociate beneficial anti-inflammatory effects from detrimental skeletal effects.
Main Methods:
- Literature review focusing on GR signaling pathways in bone.
- Analysis of gene and protein regulation by GR in osteoblasts, osteocytes, and osteoclasts.
- Examination of transcriptional mechanisms underlying proliferation, differentiation, and apoptosis.
Main Results:
- Detailed account of GR-mediated transcriptional regulation in bone cells.
- Identification of key genes and proteins involved in glucocorticoid's effects on bone.
- Understanding of how GR signaling impacts bone cell fate.
Conclusions:
- Delineating GR-mediated signaling is crucial for therapeutic advancement.
- SEGRAs hold promise for improved benefit/risk ratios in glucocorticoid therapy.
- Further research into GR pathways can mitigate glucocorticoid-induced bone loss.
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