MicroRNA‐203 mediates Porphyromonas gingivalis LPS‐induced inflammation and differentiation of periodontal ligament cells

促炎细胞因子 牙周纤维 牙龈卟啉单胞菌 化学 牙周炎 脂多糖 下调和上调 小RNA 细胞凋亡 炎症 细胞生物学 分子生物学 激活剂(遗传学) 癌症研究 免疫学 医学 内科学 生物 牙科 基因 生物化学
作者
Yang� Yang,Dongping Ren,Danyang Zhao,Bo Zhang,Rui Ye
出处
期刊:Oral Diseases [Wiley]
卷期号:29 (4): 1715-1725 被引量:5
标识
DOI:10.1111/odi.14132
摘要

In this study, we aimed to explore the effects of microRNA-203 (miR-203) on Porphyromonas gingivalis lipopolysaccharide (P.g. LPS)-stimulated periodontal ligament cells (PDLCs) and identify potential molecular targets for periodontitis treatment.Periodontal ligament cells were stimulated by P.g. LPS, followed by quantification of miR-203 and AP-1 expression. Next, loss- and gain-of-function experiments were applied in P.g. LPS-induced PDLCs. The proliferation, apoptosis, and differentiation of PDLCs were determined, and mineralized nodule numbers were counted. Functional assays were used to identify interactions among miR-203, activator protein-1 (AP-1), and intercellular adhesion molecule-1 (ICAM-1). In addition, expression of osteogenesis-related genes and release of proinflammatory factors were analyzed.miR-203 was found to be downregulated while AP-1 was upregulated in PDLCs stimulated by P.g. LPS. The overexpression of miR-203 promoted P.g. LPS-stimulated PDLC proliferation and differentiation, inhibited apoptosis, and increased the number of mineralized nodules. miR-203 was verified to downregulate AP-1/ICAM-1 axis. miR-203 overexpression reduced the secretion of proinflammatory factors while increasing the expression of osteogenesis-related genes in P.g. LPS-stimulated PDLCs, which was reversed by overexpressing AP-1 and ICAM-1.These experimental data demonstrated the potential inhibitory effects of overexpressed miR-203 on periodontitis development by promoting PDLC differentiation and suppressing inflammatory responses through AP-1/ICAM-1 axis.
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