Mechanical Induction of PGE2 in Osteocytes Blocks Glucocorticoid-Induced Apoptosis
Author Information
Author(s): Kitase Yukiko, Barragan Leonardo, Qing Hai, Kondoh Shino, Jiang Jean X, Johnson Mark L, Bonewald Lynda F
Primary Institution: Department of Oral Biology, School of Dentistry, University of Missouri at Kansas City
Hypothesis
Can mechanical loading inhibit glucocorticoid-induced osteocyte apoptosis and identify the responsible factors and molecular signaling mechanisms?
Conclusion
Mechanical loading prevents glucocorticoid-induced apoptosis in osteocytes through the release of PGE2 and activation of specific signaling pathways.
Supporting Evidence
- Mechanical loading prevents apoptosis induced by dexamethasone in osteocyte-like cells.
- PGE2 release in response to mechanical loading is protective against glucocorticoid-induced osteocyte apoptosis.
- Indomethacin, a prostaglandin synthesis inhibitor, abrogates the protective effects of mechanical loading.
- Activation of β-catenin signaling is crucial for the protective effects of PGE2.
- Fluid-flow shear stress increases the phosphorylation of glycogen synthase kinase 3, which is involved in β-catenin signaling.
Takeaway
When bones are stressed, they release a substance called PGE2 that helps keep bone cells alive, even when a medicine that usually kills them is used.
Methodology
The study used MLO-Y4 osteocyte-like cells subjected to fluid-flow shear stress and treated with dexamethasone to assess apoptosis through various assays.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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