Beijing Hanhe Daguanying Dental Clinic, No. 182 Guang'an Menwai Street, Xicheng District, 100055, Beijing, China.
Department of Stomatology, The First Medical Center of Chinese PLA General Hospital, 100853, Beijing, China.
Mol Biotechnol. 2024 Dec;66(12):3475-3484. doi: 10.1007/s12033-023-00947-0. Epub 2023 Nov 11.
Periodontitis is one of the most common complications of diabetes, which seriously affects patients' life quality. It is important to find the key factors and mechanisms to improve the treatment of periodontitis. In our study, high glucose (HG) and lipopolysaccharide (LPS) treated human periodontal ligament cells (hPDLCs) and LPS treated diabetic mice was used to establish the diabetic periodontitis model in vitro and in vivo. O-linked beta-N-acetylglucosamine glycosylation (O-GlcNAcylation) and O-linked N-acetylglucosamine transferase (OGT) protein levels were detected by western blot assay. Cell counting kit-8, alkaline phosphatase (ALP), and alizarin red staining (ARS) assays were used to observe the O-GlcNAcylation and OGT effects on cell viability and osteoblast differentiation. Co-immunoprecipitation (Co-IP) assay was used to detect the relationship between OGT and ALP. The results showed that the levels of OGT and O-GlcNAcylation were significantly increased in both cell and mouse models. ALP and ARS staining results showed that silencing of OGT or inhibition of O-glycosylation notably improved osteogenic differentiation, increased the osteoprotegerin (OPG) protein levels and decreased the receptor activator for nuclear factor-κB Ligand (RANKL) protein levels of the HG and LPS treated hPDLCs. In diabetic periodontitis mice, knockdown of OGT relieved the injury of gingival tissue, increased the ALP and OPG levels and decreased the RANKL levels. Besides, ALP interacted with OGT protein, and OGT protein was found to act on ALP serine 513 glycosylation. In conclusion, our study demonstrated that excessive O-GlcNAcylation could restrain osteoblast differentiation by O-glycosylation in ALP.
牙周炎是糖尿病最常见的并发症之一,严重影响患者的生活质量。寻找关键因素和机制来改善牙周炎的治疗方法非常重要。在我们的研究中,使用高葡萄糖(HG)和脂多糖(LPS)处理的人牙周韧带细胞(hPDLCs)和 LPS 处理的糖尿病小鼠在体外和体内建立了糖尿病牙周炎模型。通过 Western blot 检测 O-连接β-N-乙酰氨基葡萄糖糖基化(O-GlcNAcylation)和 O-连接 N-乙酰氨基葡萄糖转移酶(OGT)蛋白水平。细胞计数试剂盒-8、碱性磷酸酶(ALP)和茜素红染色(ARS)检测用于观察 O-GlcNAcylation 和 OGT 对细胞活力和成骨细胞分化的影响。通过共免疫沉淀(Co-IP)检测 OGT 和 ALP 之间的关系。结果表明,细胞和小鼠模型中 OGT 和 O-GlcNAcylation 的水平均显著升高。ALP 和 ARS 染色结果表明,沉默 OGT 或抑制 O-糖基化可显著改善成骨分化,增加骨保护素(OPG)蛋白水平,降低 HG 和 LPS 处理的 hPDLCs 中核因子-κB 受体激活剂配体(RANKL)蛋白水平。在糖尿病牙周炎小鼠中,敲低 OGT 可缓解牙龈组织损伤,增加 ALP 和 OPG 水平,降低 RANKL 水平。此外,ALP 与 OGT 蛋白相互作用,发现 OGT 蛋白作用于 ALP 丝氨酸 513 糖基化。总之,我们的研究表明,过量的 O-GlcNAcylation 可通过 ALP 上的 O-糖基化抑制成骨细胞分化。