Abstract:

Objective: To research the role of zinc finger protein 260 (Zfp260) in osteoclast differentiation under the periodontitis microenvironment.Methods: Small interfering RNA (siRNA) was transfected into the monocyte/macrophage cell line RAW264.7. The transfected cells were induced into osteoclasts by receptor activator of nuclear factor κB ligand (RANKL） for 7 days. Differentiated cells were harvested for tartrate resistant acid phosphatase (TRAP) staining. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the mRNA expression level of osteoclast differentiation-related genes. In vivo, experimental periodontitis models were established in Zfp260^flox/flox mice (Control group) and Zfp260^flox/flox Lyz2-cre^- myeloid cell conditional Zfp260-knockout mice (Zfp260^cko, Experimental group). The Micro-CT scan and histological staining were used to analyze alveolar bone resorption.Results: Zfp260 was up-regulated during osteoclast genesis. The knockdown of Zfp260 inhibited the differentiation of RAW264.7 cells into osteoclasts, and the expression of osteoclast-related factors was down-regulated (P<0.05). In vivo, the bone resorption was significantly decreased on the experimental side in Zfp260^CKO mice.Conclusion: Zfp260 regulates the osteoclast differentiation ability, which will provide a new target for solving periodontitis.

Key words: periodontitis, alveolar bone resorption, osteoclasts, zinc finger protein 260

摘要：

目的： 探究锌指蛋白260（zinc finger protein 260，Zfp260）对牙周炎破骨细胞分化的影响。方法： 将Zfp260小干扰RNA（small interfering RNA，siRNA）转染进单核/巨噬细胞系RAW264.7，转染后的细胞在核因子κB受体活化因子配体（receptor activator of nuclear factor κB ligand，RANKL）诱导7 d后，通过抗酒石酸酸性磷酸酶（tartrate resistant acid phosphatase，TRAP）染色观察破骨细胞的形成，实时定量聚合酶链反应（real-time quantitative polymerase chain reaction，RT-qPCR）检测破骨细胞分化标志基因的表达水平。基于Zfp260^flox/flox小鼠（对照组）及基因型为Zfp260^flox/flox Lyz2-cre^-的髓系细胞条件性敲除Zfp260基因（Zfp260 conditional knockout，Zfp260^CKO）小鼠（实验组）构建牙周炎模型，通过Micro-CT和组织学染色评价牙槽骨骨质破坏情况。结果： Zfp260在RAW264.7细胞向破骨细胞分化过程中表达上调；沉默Zfp260表达后，RAW264.7细胞破骨分化能力下降，破骨分化标志基因表达下调（P<0.05）；Zfp260^CKO组小鼠牙周炎侧骨吸收程度较轻。结论： Zfp260正向调控破骨细胞形成促进骨吸收，提示Zfp260可能成为牙周炎骨吸收的防治靶点。

关键词: 牙周炎, 牙槽骨吸收, 破骨细胞, 锌指蛋白260

CLC Number: 

• R782