Chemokine ligand 28 (CCL28) negatively regulates trabecular bone mass by suppressing osteoblast and osteoclast activities
Chemokine ligand 28 (CCL28) negatively regulates trabecular bone mass by suppressing osteoblast and osteoclast activities
复制标题
趋化因子配体 28 (CCL28) 通过抑制成骨细胞和破骨细胞活性来负向调节骨小梁质量
DOI：
10.1007/s00774-021-01210-9
复制
发表时间：
2021
影响因子：
3.3
通讯作者：
Yukita Akira
中科院分区：
文献类型：
--
作者：
Iwamoto Rina;Takahashi Takumi;Yoshimi Kazuto;Imai Yuji;Koide Tsuyoshi;Hara Miroku;Ninomiya Tadashi;Nakamura Hiroaki;Sayama Kazutoshi;Yukita Akira
前言骨代谢失衡会随着年龄的增长而引起骨质疏松等骨代谢疾病。虽然已知一些趋化因子参与骨量调节，但许多尚未研究。因此，本研究旨在研究趋化因子配体28（CCL 28）对骨代谢的作用。材料和方法为了研究CCL 28对骨代谢的作用，分析了10周龄雄性野生型和CCL 28敲除（CCL 28 KO）小鼠。采用骨组织形态计量学和显微计算机断层扫描技术研究Ccl 28缺乏对骨的影响。通过免疫组织化学假设CCL 28在骨组织中的定位。成骨细胞和破骨细胞标志物通过酶联免疫吸附试验和定量逆转录聚合酶链反应进行评价。最后，在体外实验中使用MC 3 T3-E1和骨髓巨噬细胞揭示了直接的影响，CCL 28对成骨细胞和破骨细胞。ResultsThis study showed thatCCL 28 deficiency significantly increased bone mass and number of mature osteoblasts.在骨组织上的成骨细胞和破骨细胞中观察到CCL 28的免疫反应性。此外，Ccl 28缺陷促进成骨细胞和破骨细胞的成熟。此外，CCL 28治疗降低成骨细胞和破骨细胞的活动，但不影响differentiation.ConclusionIn总结，这项研究表明，CCL 28是通过抑制成骨细胞和破骨细胞的活动的骨量负调节器之一。这些结果为骨免疫学和选择新的骨质疏松症治疗方法提供了重要的见解。
IntroductionBone 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 methodsTo investigate the role of CCL28 on bone metabolism, 10-week-old male wild-type andCcl28knockout (Ccl28KO) mice were analyzed. Microcomputed tomography analysis and bone tissue morphometry were used to investigate the effect ofCcl28deficiency 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.ResultsThis study showed thatCcl28deficiency significantly increased bone mass and the number of mature osteoblasts. Immunoreactivity for CCL28 was observed in osteoblasts and osteoclasts on bone tissue. Additionally,Ccl28deficiency promoted osteoblast and osteoclast maturation. Moreover, CCL28 treatment decreased osteoblast and osteoclast activities but did not affect differentiation.ConclusionIn 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.