Department of Endodontics, the First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China.
Department of General Surgery, the Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China; Department of General Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China.
Int Immunopharmacol. 2021 Feb;91:107275. doi: 10.1016/j.intimp.2020.107275. Epub 2020 Dec 21.
Periodontitis is a common chronic disease. Osteoclast differentiation contributes to alveolar bone resorption which is a distinct phenomenon during periodontitis. Syndecan 4 (SDC4), a member of the syndecan family, was found to be highly expressed during periodontitis. However, little is known about its role in periodontitis. Herein, we explored the role of SDC4 in osteoclast differentiation. An experimental periodontitis rat model was established by ligating the right first molar. The SDC4 expression in periodontium was detected by western blot and immunofluorescence. Our study demonstrated that SDC4 was highly expressed in the periodontium of periodontitis rats. It was positively transcriptionally regulated by NF-κB. SDC4 silencing abrogated osteoclast differentiation induced by RANKL, while SDC4 overexpression enhanced osteoclast differentiation. Moreover, SDC4 enhanced autophagy induced by RANKL. 3-MA, an autophagy inhibitor, was employed to explore whether SDC4 impacts osteoclast differentiation through activating autophagy. Treatment with 3-MA abolished osteoclast differentiation which was enhanced by SDC4, indicating that SDC4 promotes osteoclast differentiation through activating autophagy. This study reveals that SDC4 may contribute to osteoclast differentiation during periodontitis through activating autophagy. It sheds light on the important role of SDC4 in periodontitis.
牙周炎是一种常见的慢性疾病。破骨细胞分化导致牙槽骨吸收，这是牙周炎的一个显著现象。黏附素 4（SDC4）是黏附素家族的一员，在牙周炎中表达水平较高。然而，关于其在牙周炎中的作用知之甚少。在此，我们探讨了 SDC4 在破骨细胞分化中的作用。通过结扎右侧第一磨牙建立实验性牙周炎大鼠模型。通过 Western blot 和免疫荧光检测牙周组织中 SDC4 的表达。我们的研究表明，SDC4 在牙周炎大鼠的牙周组织中高度表达。它受 NF-κB 的正向转录调控。SDC4 沉默可阻断 RANKL 诱导的破骨细胞分化，而 SDC4 过表达则增强破骨细胞分化。此外，SDC4 增强了 RANKL 诱导的自噬。我们采用自噬抑制剂 3-MA 来探讨 SDC4 是否通过激活自噬来影响破骨细胞分化。3-MA 处理可消除 SDC4 增强的破骨细胞分化，表明 SDC4 通过激活自噬促进破骨细胞分化。本研究揭示 SDC4 可能通过激活自噬促进牙周炎中的破骨细胞分化。它揭示了 SDC4 在牙周炎中的重要作用。
