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Updated: Apr 16, 2026
A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
Published on: March 15, 2018
Transmembrane protein 173 inhibits RANKL-induced osteoclast differentiation
Chung-Hyeon Choe1, In Sun Park2, Jisang Park3
1Jeonju Biomaterials Institute, Jeonju 561-360, Republic of Korea; Department of Molecular Biology and the Institute for Molecular Biology and Genetics, Chonbuk National University, Jeonju 561-756, Republic of Korea.
Abstract:
Tmem173 was identified as a growth inhibitor associated with major histocompatibility complex (MHC) class II and a potential stimulator for IFN-β, an innate immune inducer and a negative feedback controller for RANKL-induced osteoclast differentiation of monocytic macrophage cells. In this study, we confirmed that transmembrane protein 173 (Tmem173) overexpression inhibited the expression of osteoclast-specific genes, tartrate-resistant acid phosphatase (TRAP), cathepsin K, and matrix metalloproteinase-9 (MMP-9), as well as bone resorption pit formation in RANKL-treated RAW 264.7 cells. Activation of osteoclast-specific transcription factors, c-Fos and nuclear factor of activated T cells cytoplasmic-1 (NFATc1), and RANKL-induced activation of ERK were also down-regulated by Tmem173 overexpression. Collectively, these results suggest that Tmem173 plays a regulatory role in RANKL-RANK-mediated signaling in osteoclastogenesis.
Insights
Transmembrane protein 173 (Tmem173) inhibits osteoclast differentiation by down-regulating key genes and transcription factors. This finding reveals Tmem173
Area of Science:
- Immunology
- Cell Biology
- Bone Biology
Background:
- Transmembrane protein 173 (Tmem173) is linked to MHC class II and may modulate innate immunity via IFN-β.
- Tmem173 is a potential negative regulator of osteoclast differentiation induced by RANKL.
- Osteoclasts are crucial for bone remodeling and their dysregulation contributes to bone diseases.
Purpose of the Study:
- To investigate the role of Tmem173 in regulating osteoclast differentiation.
- To elucidate the molecular mechanisms by which Tmem173 affects osteoclastogenesis.
Main Methods:
- Overexpression of Tmem173 in RAW 264.7 cells.
- Assessment of osteoclast-specific gene expression (TRAP, cathepsin K, MMP-9).
- Analysis of bone resorption pit formation.
- Evaluation of transcription factor activation (c-Fos, NFATc1) and signaling pathways (ERK).
Main Results:
- Tmem173 overexpression significantly inhibited osteoclast-specific gene expression and bone resorption.
- Tmem173 suppressed the activation of key osteoclastogenic transcription factors, c-Fos and NFATc1.
- Tmem173 down-regulated RANKL-induced ERK activation.
Conclusions:
- Tmem173 acts as an inhibitor of osteoclast differentiation.
- Tmem173 negatively regulates RANKL-RANK signaling pathways involved in osteoclastogenesis.
- Tmem173 represents a potential therapeutic target for bone diseases characterized by excessive osteoclast activity.
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