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Updated: Nov 12, 2025

Osteoclast Derivation from Mouse Bone Marrow
Published on: November 6, 2014
Chemokine ligand 28 (CCL28) negatively regulates trabecular bone mass by suppressing osteoblast and osteoclast
Rina Iwamoto1, Takumi Takahashi2, Kazuto Yoshimi3
1Department of Bioscience, Graduate School of Science and Technology, Shizuoka University, 836 Ohya, Suruga-ku, Shizuoka, 422-8529, Japan.
Introduction:
Bone metabolism imbalances cause bone metabolism diseases, like osteoporosis, through aging. Although some chemokines are known to be involved in bone mass regulation, many have not been investigated. Thus, the present study aimed to investigate the role of chemokine ligand 28 (CCL28) on bone metabolism.
Materials And Methods:
To investigate the role of CCL28 on bone metabolism, 10-week-old male wild-type and Ccl28 knockout (Ccl28 KO) mice were analyzed. Microcomputed tomography analysis and bone tissue morphometry were used to investigate the effect of Ccl28 deficiency on the bone. CCL28 localization in bone tissue was assumed by immunohistochemistry. Osteoblast and osteoclast markers were evaluated by enzyme-linked immunosorbent assay and quantitative reverse transcription-polymerase chain reaction. Finally, in vitro experiments using MC3T3-E1 and bone marrow macrophages revealed the direct effect of CCL28 on osteoblast and osteoclast.
Results:
This study showed that Ccl28 deficiency significantly increased bone mass and the number of mature osteoblasts. Immunoreactivity for CCL28 was observed in osteoblasts and osteoclasts on bone tissue. Additionally, Ccl28 deficiency promoted osteoblast and osteoclast maturation. Moreover, CCL28 treatment decreased osteoblast and osteoclast activities but did not affect differentiation.
Conclusion:
In summary, this study indicated that CCL28 is one of the negative regulators of bone mass by suppressing osteoblast and osteoclast activities. These results provide important insights into bone immunology and the selection of new osteoporosis treatments.
Insights
Chemokine ligand 28 (CCL28) negatively regulates bone mass by suppressing osteoblast and osteoclast activity. This finding offers new therapeutic targets for osteoporosis and bone metabolism diseases.
Area of Science:
- Bone biology
- Immunology
- Metabolic diseases
Background:
- Bone metabolism imbalances contribute to age-related diseases like osteoporosis.
- While some chemokines are implicated in bone regulation, many remain unstudied.
- The role of chemokine ligand 28 (CCL28) in bone metabolism requires investigation.
Purpose of the Study:
- To elucidate the function of CCL28 in regulating bone metabolism.
- To determine the impact of CCL28 deficiency on bone mass and cellular activity.
Main Methods:
- Analysis of wild-type and Ccl28 knockout mice using microcomputed tomography and bone morphometry.
- Immunohistochemistry to localize CCL28 in bone tissue.
- Enzyme-linked immunosorbent assay and qRT-PCR for osteoblast and osteoclast markers.
- In vitro studies with MC3T3-E1 and bone marrow macrophages to assess direct CCL28 effects.
Main Results:
- Ccl28 deficiency significantly increased bone mass and osteoblast numbers.
- CCL28 was localized to osteoblasts and osteoclasts.
- Ccl28 deficiency enhanced osteoblast and osteoclast maturation.
- CCL28 treatment inhibited osteoblast and osteoclast activity without affecting differentiation.
Conclusions:
- CCL28 acts as a negative regulator of bone mass by inhibiting osteoblast and osteoclast activity.
- These findings contribute to understanding bone immunology.
- CCL28 presents a potential target for novel osteoporosis treatments.
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