Wnt信号通路
牙周纤维
体内
牙龈卟啉单胞菌
牙周炎
干瘪的
炎症
化学
LRP5
脂多糖
药理学
信号转导
细胞生物学
医学
内科学
生物
牙科
生物技术
作者
Fan Yang,Dingming Huang,Liangzhi Xu,Wei Xu,Xiaowei Yi,Xuedong Zhou,L. Ye,Lan Zhang
摘要
To explore the mechanism of secreted frizzled-related protein I (sFRP1) involvement in the osteogenic differentiation of human periodontal ligament cells (hPDLCs) under inflammatory conditions.hPDLCs were cultured in an osteogenic differentiation-inducing medium (odi) and subjected to the stimulation of Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS) with or without the inhibition of sFRP1. Quantitative real-time polymerase chain reaction, Western blot and enzyme-linked immunosorbent assay were carried out to evaluate the expression of osteogenic markers as well as the classic Wnt signalling pathway. Periapical periodontitis was induced in Wistar rats to further confirm the effect of sFRP1 inhibitor on bone loss in vivo. After the Shapiro-Wilk normality test, data were analysed by Student's paired t-test or one-way Anova test with a P value less than 0.05 as the level of statistical significance.Significantly decreased mRNA and protein expression of osteogenic markers were detected in hPDLCs treated with P. gingivalis LPS during osteogenic induction (P < 0.001). Increased expression of sFRP1 was observed (P < 0.01), whilst Wnt/β-catenin signalling pathway was inhibited by the addition of P. gingivalis LPS (P < 0.01). After the addition of the sFRP1 inhibitor, the decrease of osteogenic markers (P < 0.05) and the inhibition of Wnt/β-catenin signalling pathway (P < 0.05) were reversed significantly. The animal experiment further confirmed that the sFRP1 inhibitor significantly reduced bone loss of periapical lesions in vivo (P < 0.0001).Wnt antagonist sFRP1 was involved in the osteogenic differentiation of hPDLCs under inflammation. Modulation of the Wnt/β-catenin signalling pathway through the inhibition of sFRP1 may offer a new perspective on the treatment of chronic apical periodontitis.
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