Zheng Junyi, Zhang Pingying, Xie Huimin, Chu Zhengyi, Xu Baohua
Oral Medicine Department, China-Japan Friendship Hospital, No. 2, Yinghua Garden East Street, Chaoyang District, Beijing, 100029, China.
Qingdao Traditional Chinese Medicine Hospital, Qingdao Hiser Hospital Affiliated of Qingdao University, Qingdao, 266000, China.
Odontology. 2025 Aug 25. doi: 10.1007/s10266-025-01176-4.
To explore the role and mechanism of long non-coding RNA SLC7A11-AS1 in lipopolysaccharide-induced injury of human periodontal ligament stem cells (hPDLSCs) via regulation of microRNA-1260 (miR-1260), and to assess its diagnostic value in periodontitis. Serum levels of SLC7A11-AS1 and miR-1260 were measured by qRT-PCR in 80 periodontitis patients and 80 healthy controls. Diagnostic performance was evaluated using receiver operating characteristic (ROC) analysis and correlation with periodontal indices. hPDLSCs were treated with 2 µg/mL LPS to induce inflammation; SLC7A11-AS1 was silenced by siRNA and miR-1260 inhibited by inhibitor. Cell viability, apoptosis, expression of Cyclin D1, Bcl-2, and Bax, inflammatory cytokines, and oxidative stress markers were assessed. Direct interaction was confirmed by dual-luciferase reporter assay. Serum SLC7A11-AS1 was up-regulated in periodontitis (P < 0.001) with high diagnostic accuracy (AUC = 0.8047) and positive correlation with PLI, SBI, PD, and AL (r = 0.716-0.740, P < 0.001). miR-1260 was down-regulated and inversely correlated with SLC7A11-AS1 (r = -0.713, P < 0.001). In hPDLSCs, LPS induced SLC7A11-AS1 expression, reduced viability, increased apoptosis, and altered Cyclin D1, Bcl-2, and Bax levels; these effects were reversed by SLC7A11-AS1 knockdown and reinstated by miR-1260 inhibition. SLC7A11-AS1 sponged miR-1260, modulating inflammatory and oxidative responses. SLC7A11-AS1 exacerbates LPS-induced hPDLSC injury by negatively regulating miR-1260, representing a potential biomarker and therapeutic target in periodontitis.
通过调控微小RNA-1260（miR-1260）探讨长链非编码RNA SLC7A11-AS1在脂多糖诱导的人牙周膜干细胞（hPDLSCs）损伤中的作用及机制，并评估其在牙周炎中的诊断价值。采用qRT-PCR检测80例牙周炎患者和80例健康对照者血清中SLC7A11-AS1和miR-1260的水平。使用受试者工作特征（ROC）分析评估诊断性能，并分析其与牙周指数的相关性。用2 μg/mL脂多糖处理hPDLSCs以诱导炎症；用小干扰RNA（siRNA）沉默SLC7A11-AS1，用抑制剂抑制miR-1260。评估细胞活力、凋亡、细胞周期蛋白D1、Bcl-2和Bax的表达、炎性细胞因子和氧化应激标志物。通过双荧光素酶报告基因检测证实直接相互作用。牙周炎患者血清SLC7A11-AS1上调（P＜0.001），诊断准确性高（曲线下面积[AUC]=0.8047），且与菌斑指数（PLI）、牙龈出血指数（SBI）、牙周袋深度（PD）和牙槽骨吸收（AL）呈正相关（r=0.716-0.740，P＜0.001）。miR-1260下调，且与SLC7A11-AS1呈负相关（r=-0.713，P＜0.001）。在hPDLSCs中，脂多糖诱导SLC7A11-AS1表达，降低细胞活力，增加凋亡，并改变细胞周期蛋白D1、Bcl-2和Bax水平；SLC7A11-AS1敲低可逆转这些作用，而miR-1260抑制可恢复这些作用。SLC7A11-AS1可吸附miR-1260，调节炎症和氧化反应。SLC7A11-AS1通过负向调节miR-1260加重脂多糖诱导的hPDLSC损伤，是牙周炎潜在的生物标志物和治疗靶点。
