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A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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Characterization of a spontaneous osteopetrosis model using RANKL-dysfunctional mice
Beom Chang Kim1, Gwangchul Lee2, Yuria Jang1
1Laboratory of Orthopedic Research, Chosun University Hospital, Republic of Korea; Departments of Premedical Science, College of Medicine, Chosun University, Gwangju 61452, Republic of Korea.
Tissue & Cell
|May 22, 2024
Summary
Mice with a mutation in the tumor necrosis factor superfamily member 11 (TNFSF11) gene show bone resorption instability. This Tnfsf11 mutation model is valuable for studying bone biology and related diseases.
Area of Science:
- Bone Biology
- Genetics
- Animal Models
Background:
- Receptor activator of nuclear factor-κB ligand (RANKL), encoded by TNFSF11, is vital for osteoclast function and bone remodeling.
- Mouse models are essential for investigating genetic mechanisms in bone diseases.
Purpose of the Study:
- To evaluate the Tnfsf11gum mouse model for understanding bone remodeling and dysmorphology.
- To investigate the genetic landscape of TNFSF11 inactivation in bone marrow.
Main Methods:
- Utilized Tnfsf11gum/+ and Tnfsf11+/+ mice.
- Employed Micro-CT, ELISA, histological evaluation, and RNA-sequencing.
- Analyzed bone marrow tissues for genetic and cellular changes.
Main Results:
- Tnfsf11gum/+ mice displayed severe osteopetrosis and reduced osteoclast numbers.
- Serum RANKL levels were significantly lower in mutant mice.
- Differential gene expression observed in pathways related to osteoblast and osteoclast activity.
Conclusions:
- A heterozygous Tnfsf11 mutation causes bone resorption instability.
- This mouse model is suitable for bone resorption research.
- The mutation impacts bone remodeling without drastically altering osteoblast/osteoclast gene expression.
