Porphyromonas gingivalis LPS-stimulated BMSC-derived exosome promotes osteoclastogenesis via miR-151-3p/PAFAH1B1.

IF 2.9 3区医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Oral diseases Pub Date : 2025-01-01 Epub Date: 2024-06-24 DOI:10.1111/odi.15031

Jia-Chen Dong, Yue Liao, Wei Zhou, Meng-Jun Sun, Huan-Yu Zhang, Yan Li, Zhong-Chen Song

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Abstract

Objectives: Porphyromonas gingivalis-LPS regulated bone metabolism by triggering dysfunction of osteoblasts directly, and affecting activity of osteoclasts through intracellular communication. Exosome, as the mediator of intercellular communication, was important vesicle to regulate osteogenesis and osteoclastogenesis. This research was designed for investigating the mechanism of BMSCs-EXO in modulating osteoclastic activity under the P. gingivalis-LPS.

Materials and methods: The cytotoxicity and osteogenic effects of P. gingivalis-LPS on BMSCs was evaluated, and then osteoclastic activity of RAW264.7 co-cultured with exosomes was detected. Besides, Affymetrix miRNA array and luciferase reporter assay were used to identify the target exosomal miRNA signal pathway.

Results: BMSCs' osteogenic differentiation and proliferation were decreased under 1 and 10 μg/mL P. gingivalis-LPS. Osteoclastic-related genes and proteins levels were promoted by P. gingivalis-LPS-stimulated BMSCs-EXO. Based on the miRNA microarray analysis, exosomal miR-151-3p was lessened in BMExo-LPS group, which facilitated osteoclastic differentiation through miR-151-3p/PAFAH1B1.

Conclusions: Porphyromonas gingivalis-LPS could regulated bone metabolism by inhibiting proliferation and osteogenesis of BMSCs directly. Also, P. gingivalis-LPS-stimulated BMSCs-EXO promoted osteoclastogenesis via activating miR-151-3p/PAFAH1B1 signal pathway.

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牙龈卟啉菌LPS刺激的BMSC衍生外泌体通过miR-151-3p/PAFAH1B1促进破骨细胞生成

目的：牙龈卟啉单胞菌（Porphyromonas gingivalis）-LPS通过直接引发成骨细胞功能障碍和通过细胞内通讯影响破骨细胞活性来调节骨代谢。外泌体作为细胞间通讯的媒介，是调控成骨和破骨细胞生成的重要囊泡。本研究旨在探讨 BMSCs-EXO 在 P. gingivalis-LPS 作用下调节破骨细胞活性的机制：评估了牙龈脓毒性-LPS 对 BMSCs 的细胞毒性和成骨效应，然后检测了与外泌体共培养的 RAW264.7 的破骨活性。此外，还利用Affymetrix miRNA阵列和荧光素酶报告实验确定了外泌体miRNA的靶信号通路：结果：在 1 和 10 μg/mL P. gingivalis-LPS 作用下，BMSCs 的成骨分化和增殖能力下降。破骨细胞相关基因和蛋白水平在 P. gingivalis-LPS 刺激的 BMSCs-EXO 中得到促进。根据 miRNA 微阵列分析，BMExo-LPS 组的外泌体 miR-151-3p 减少，这通过 miR-151-3p/PAFAH1B1 促进了破骨细胞的分化：结论：牙龈卟啉菌-LPS可直接抑制BMSCs的增殖和成骨，从而调节骨代谢。结论：牙龈卟啉菌-LPS 可通过直接抑制 BMSCs 的增殖和成骨来调节骨代谢，同时，牙龈卟啉菌-LPS 刺激的 BMSCs-EXO 可通过激活 miR-151-3p/PAFAH1B1 信号通路促进破骨细胞生成。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Oral diseases 医学-牙科与口腔外科

CiteScore

7.60

自引率

5.30%

发文量

325

审稿时长

4-8 weeks

期刊介绍： Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.