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Mechanotransduction in bone does not require a functional cyclooxygenase-2 (COX-2) gene
Imranul Alam1, Stuart J Warden, Alexander G Robling
1Department of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Summary
A functional cyclooxygenase-2 (COX-2) gene is not required for bone mechanotransduction. This is likely due to compensatory COX-1 activity in COX-2 deficient mice, which impacts bone mass and mechanical properties.
Area of Science:
- Skeletal biology
- Biochemistry
- Genetics
Background:
- Cyclooxygenase-2 (COX-2) is implicated in bone's response to mechanical loading.
- Pharmacological COX-2 inhibition reduces mechanically induced bone formation.
- The necessity of COX-2 for skeletal mechanotransduction remains unclear.
Purpose of the Study:
- To investigate the role of COX-2 in skeletal mechanotransduction using a genetic approach.
- To compare the skeletal responsiveness of COX-2 deficient mice (COX-2(-/-)) and wildtype controls (COX-2(+/+)).
Main Methods:
- Adult female COX-2(-/-) and COX-2(+/+) mice were subjected to ulna axial loading.
- Histomorphometry was used to assess the bone's response to loading.
- Femur phenotype and COX-1 expression via real-time RT-PCR were analyzed.
Main Results:
- COX-2(-/-) mice exhibited reduced bone mass and altered architecture, though some differences were weight-dependent.
- No significant histomorphometric differences in response to mechanical loading were observed between genotypes.
- COX-2(-/-) mice showed significantly increased COX-1 expression in loaded ulnas compared to controls.
Conclusions:
- A functional COX-2 gene is not essential for skeletal mechanotransduction.
- Mechanically induced COX-1 expression may compensate for the absence of COX-2.
- Findings contrast with previous pharmacological studies on COX-2's role in bone loading response.