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Reduced bone mineral density in SOCS-2-deficient mice
Mattias Lorentzon1, Chris J Greenhalgh, Subburaman Mohan
1Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Sahlgrenska University Hospital, Gothenburg University, 41345 Gothenburg, Sweden. Mattias.Lorentzon@medic.gu.se
Pediatric Research
|December 9, 2004
Summary
Suppressor of cytokine signaling-2 (SOCS-2) deficiency reduces bone mineral density in mice. This finding contrasts with previous observations of increased skeletal growth, suggesting complex regulatory roles for SOCS-2 in bone homeostasis.
Area of Science:
- Endocrinology
- Bone Biology
- Molecular Biology
Background:
- Suppressor of cytokine signaling-2 (SOCS-2) negatively regulates cytokine signaling via the JAK/STAT pathway.
- Previous studies linked SOCS-2 deficiency to increased longitudinal skeletal growth and deregulated GH/IGF-I signaling.
Purpose of the Study:
- To investigate the role of SOCS-2 in the regulation of bone mineral density (BMD).
Main Methods:
- Dual x-ray absorptiometry (DXA) was used to assess areal BMD.
- Peripheral quantitative computerized tomography (pQCT) was employed to measure volumetric BMD and cortical bone parameters.
Main Results:
- SOCS-2 knockout (SOCS-2-/-) mice exhibited reduced tibial areal BMD at both 4 and 15 weeks of age.
- pQCT revealed decreased trabecular volumetric BMD in the distal femur and reduced cortical volumetric BMD in the tibia of SOCS-2-/- mice.
- Cortical cross-sectional area was diminished in young (4-wk-old) but not older (15-wk-old) SOCS-2-/- mice.
Conclusions:
- SOCS-2 inactivation leads to reduced trabecular and cortical volumetric BMD.
- The observed reduction in BMD is not explained by enhanced GH/IGF-I signaling, indicating an unknown mechanism.
- Further research is needed to elucidate the precise mechanisms underlying SOCS-2's role in bone mineral density regulation.