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Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation
Published on: August 23, 2018
Human bone marrow adipocytes support dexamethasone-induced osteoclast differentiation and function through RANKL
Hisataka Goto1, Makoto Osaki, Tatsuya Fukushima
1Department of Orthopaedic Surgery, Graduate School of Biomedical Science, Nagasaki University, Japan.
Biomedical Research (Tokyo, Japan)
|March 9, 2011
Summary
Human bone marrow adipocytes promote osteoclast differentiation and bone resorption. Dexamethasone treatment increased Receptor Activator of Nuclear factor κ B Ligand (RANKL) expression, driving this effect.
Area of Science:
- Bone Biology
- Endocrinology
- Cell Biology
Background:
- Receptor Activator of Nuclear factor κ B Ligand (RANKL) is crucial for bone remodeling and osteoclastogenesis.
- The role of bone marrow adipocytes in regulating RANKL and bone metabolism is not fully understood.
Purpose of the Study:
- To investigate RANKL regulation in primary human bone marrow adipocytes.
- To determine the relationship between bone marrow adipocytes and bone metabolism.
Main Methods:
- Primary human bone marrow adipocytes were treated with dexamethasone.
- Co-culture systems of osteoclast precursors and bone marrow adipocytes were utilized.
- RANKL expression and osteoclast differentiation/activity were assessed.
Main Results:
- Dexamethasone increased RANKL expression and the RANKL/osteoprotegerin (OPG) mRNA ratio in marrow adipocytes.
- Co-cultured bone marrow adipocytes promoted osteoclast precursor differentiation and bone resorption.
- RANKL antibody treatment inhibited these effects, and cell-to-cell contact was necessary.
Conclusions:
- Primary human bone marrow adipocytes can promote osteoclast differentiation and activity.
- Adipocytes contribute to bone metabolism regulation via RANKL, similar to osteoblasts.
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