Department of Orthodontics, Osaka Dental University, 8-1 Kuzuhahanazonocho, Hirakata, Japan.
Cell Biol Int. 2014 Jun;38(6):723-8. doi: 10.1002/cbin.10263. Epub 2014 Feb 21.
Osteoclast differentiation/activation is involved in orthodontic tooth movement at the compression sites of the alveolar bone. RANKL, a member of the TNF family expressed in osteoblasts, binds to RANK, a member of the TNF receptor family expressed on preosteoclasts, resulting in differentiation of preosteoclasts into mature osteoclasts. Several members of the TNF family, such as TNF and Fas ligand, can induce apoptosis by activation of caspase-3. We have investigated whether caspase-3 be involved in the late stage of RANKL-induced osteoclast differentiation. Increased active caspase-3 was found in mouse monocytic RAW264 cells differentiated into mature osteoclasts by treatment with RANKL for 3 days. Co-treatment with Z-Asp-CH₂-DCB, a caspase-3-specific inhibitor, augmented RANKL-induced osteoclast differentiation in RAW264 cells, also seen in mouse bone marrow macrophages. This suggests that activation of caspase-3 may play an inhibitory role at the late stage of RANKL-induced osteoclast differentiation.
破骨细胞分化/激活参与牙槽骨压缩部位的正畸牙齿移动。RANKL，一种在成骨细胞中表达的 TNF 家族成员，与 RANK，一种在破骨前体细胞中表达的 TNF 受体家族成员结合，导致破骨前体细胞分化为成熟的破骨细胞。TNF 家族的几个成员，如 TNF 和 Fas 配体，可通过激活 caspase-3 诱导细胞凋亡。我们研究了 caspase-3 是否参与 RANKL 诱导的破骨细胞分化的晚期。用 RANKL 处理 3 天可诱导小鼠单核细胞 RAW264 细胞分化为成熟破骨细胞，在此过程中发现活性 caspase-3 增加。用 caspase-3 特异性抑制剂 Z-Asp-CH₂-DCB 共处理 RAW264 细胞和小鼠骨髓巨噬细胞，可增强 RANKL 诱导的破骨细胞分化。这表明 caspase-3 的激活可能在 RANKL 诱导的破骨细胞分化的晚期发挥抑制作用。
