牙周炎
破骨细胞
炎症
骨吸收
MMP9公司
促炎细胞因子
生物
免疫学
下调和上调
细胞生物学
癌症研究
医学
内分泌学
内科学
受体
基因
生物化学
作者
Jie Guo,Xuemin Zeng,Jie Miao,Chunpeng Liu,Fulan Wei,Dongxu Liu,Zhong Zheng,Kang Ting,Chunling Wang,Yi Liu
摘要
Periodontitis is a multiple infection and inflammatory disease featured by connective tissue homeostasis loss, periodontal inflammation, and alveolar bone resorption. MicroRNAs (miRNAs) are involved in the mediation of a large scale of pathological processes. Here, we show that miRNA-218 provides protective effect on periodontitis via regulation of matrix metalloproteinase-9 (Mmp9). This pathway is aberrant in periodontium from rats with periodontitis and human periodontal ligament progenitor cells stimulated by lipopolysaccharide, with downregulation of miR-218 and higher levels of Mmp9 compared with periodontium from healthy rats and cells without stimulation. Overexpression of miR-218 can suppress the degradation of Collagen Types I and IV and dentin sialoprotein (DSP), attenuate osteoclast formation, and inhibit the secretion of proinflammatory cytokines. On the other hand, overexpression of Mmp9 promotes the degradation of Collagen Types I and IV and DSP as well as RANKL-induced osteoclast formation and elevates inflammatory factors levels. Furthermore, the inhibitory effect of miR-218 was prevented by rescuing the Mmp9 expression. In addition, we also have showed that miR-218 was able to attenuate bone resorption and inflammation in a periodontitis rat model. Collectively, our findings therefore suggest that miR-218 acts as a protective role in periodontitis through the regulation of Mmp9.
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