牙周炎
成骨细胞
骨吸收
牙槽
牙周纤维
细胞凋亡
巨噬细胞
破骨细胞
化学
细胞生物学
吸收
体外
癌症研究
医学
病理
生物
内科学
牙科
生物化学
作者
Xu Liu,Lijia Guo,Juan Du,Zhenhua Luo,Junji Xu,Ujjal K. Bhawal,Xiaoyan Li,Yi Liu
出处
期刊:Oral Diseases
[Wiley]
日期:2023-11-22
卷期号:30 (5): 3296-3307
被引量:6
摘要
Abstract Objectives Periodontitis is induced by the imbalance between osteoblast and osteoclast activity, which leads to periodontal tissue destruction. Macrophages play a vital role in periodontitis. However, the hypoxic periodontal environment will also induce macrophage apoptosis within a short time. Apoptotic bodies (ABs) are the major products generated from apoptotic cells, but whether macrophage‐derived ABs play a regulatory role as their mother cells in periodontitis remains unknown. In the present study, we aimed to investigate the effects of ABs on osteoblasts. Method ABs derived from hypoxia‐induced macrophages were co‐cultured with osteoblasts and the impact of ABs on osteoblast differentiation in vitro was assessed. In vivo, periodontitis model was established and macrophages‐derived ABs were injected into the gingival sulcus. The effects of ABs on periodontal bone resorption were determined. Results The results showed that ABs significantly inhibit osteoblast differentiation and promoted alveolar bone resorption in periodontitis. MicroRNA (miRNAs) array analysis was performed and revealed that miR‐483‐5p is the key miRNA in ABs. Dual luciferase reporter assays were performed and confirmed that miR‐483‐5p targeted Col1A1 mRNA and attenuated its expression. Conclusion Macrophage‐derived ABs inhibit osteoblast differentiation via the transfer of miR‐483‐5p, which downregulates Col1A1 expression and finally suppresses osteogenic activity.
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