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Hypoxia mediates osteocyte ORP150 expression and cell death in vitro
Monica Montesi1, Katharina Jähn2, Lynda Bonewald2
1Medical Technology Laboratory, Rizzoli Orthopaedic Institute, I‑40136 Bologna, Italy.
Molecular Medicine Reports
|October 26, 2016
Summary
Skeletal unloading causes bone loss via hypoxia. This study found that oxygen-regulated protein 150 (ORP150) mRNA increased in osteocytes under hypoxic conditions, potentially protecting cells from death.
Area of Science:
- Bone biology
- Cellular adaptation to hypoxia
- Mechanotransduction
Background:
- Skeletal unloading induces bone hypoxia, favoring resorption over remodeling.
- Osteocytes, bone's mechanosensors, are crucial for bone homeostasis.
- Hypoxia triggers osteocyte apoptosis or osteoclast stimulation.
Purpose of the Study:
- To investigate the role of Oxygen-regulated protein 150 (ORP150) in osteocytes under hypoxic conditions.
- To test the hypothesis that ORP150 expression increases in osteocytes during hypoxia.
Main Methods:
- MLO-Y4 osteocyte cell line cultured under normoxic and hypoxic (1% O2) conditions for up to 72 hours.
- Assessment of hypoxia induction, cell viability, cell death, apoptosis, and ORP150 mRNA and protein expression.
Main Results:
- 1% O2 significantly induced hypoxia, reduced cell number, and increased cell death and apoptosis.
- ORP150 mRNA levels were significantly higher in hypoxic conditions at 72 hours.
- No significant difference in ORP150 protein expression was observed between normoxic and hypoxic groups.
Conclusions:
- Hypoxia induces significant cellular stress and apoptosis in osteocytes.
- Increased ORP150 mRNA under hypoxia may indicate a cytoprotective response.
- Further research is needed to clarify ORP150's role in osteocyte survival during unloading-induced hypoxia.
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