Chemokine ligand 28 (CCL28) negatively regulates trabecular bone mass by suppressing osteoblast and osteoclast activities
Rina Iwamoto, Takumi Takahashi, Kazuto Yoshimi, Yuji Imai, Tsuyoshi Koide, Miroku Hara, Tadashi Ninomiya, Hiroaki Nakamura, Kazutoshi Sayama, Akira Yukita
Journal of Bone and Mineral Metabolism 2021 March 15 DOI:10.1007/s00774-021-01210-9
Healthy adult bone mass is tightly controlled by regulator of bone formation and resorption (bone metabolism regulator). The disturbance of this regulation causes pathological bone loss, such as osteoporosis. Recently, the relationship between many chemokines and bone has not yet been investigated, although chemokine has been attracting attention as a bone metabolism regulator.
We performed experiments to clarify the role of CCL28 in bone metabolism, because CCR3 which receptor for CCL28, regulates bone metabolism.
Analysis of Ccl28 deficient mice bone tissue and cultured cell experiments revealed that CCL28 negatively regulates bone mass via suppresses the activation of osteoblasts and osteoclasts. Interestingly, we revealed that Ccl28 expression increased in aged mice bone tissue.
These results provide important insights into bone immunology and the selection of new osteoporosis treatments.
Figure: (a)μCT analysis of bone structure revealed that Ccl28 deficiency increased trabecular bone mass. (b)In vivo and In vitro experiments revealed that CCL28 negatively regulates bone mass by suppressing the activation of osteoblasts and osteoclasts in bone tissue.