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外膜囊泡通过血清淀粉样蛋白A3/ Toll样受体4/髓样分化因子88/核因子κB轴抑制骨髓间充质干细胞的成骨分化。

OMVs inhibit osteogenic differentiation of BMSCs via SAA3/TLR4/MyD88/NF-κB axis.

作者信息

Yan Yongyong, Wang Haiyan, Deng Huizhi, He Haokun, Ge Qing, Zha Jun, Chen Jun, Zhang Qing, Deng Haiyan, Wu Gang, Jaspers Richard T, Pathak Janak L

机构信息

School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction & Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, China.

Laboratory for Myology, Department of Human Movement Sciences, Faculty of Behavioural and Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam Movement Sciences, Amsterdam, the Netherlands.

出版信息

J Oral Microbiol. 2025 Aug 8;17(1):2540823. doi: 10.1080/20002297.2025.2540823. eCollection 2025.

DOI:10.1080/20002297.2025.2540823
PMID:40791819
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12337729/
Abstract

BACKGROUNDS: Periodontitis-induced alveolar bone loss is a primary cause of tooth loss. () is the primary pathogenic bacterium of periodontitis. Outer membrane vesicles (OMVs) derived from (-OMVs) contain various bioactive molecules, and several studies have suggested that -OMVs may participate in alveolar bone loss caused by periodontitis. MATERIALS AND METHODS: -OMVs were isolated and characterized. The effect of -OMVs on BMSCs proliferation and osteogenic differentiation was analyzed. High-throughput sequencing, RT-qPCR, and Western blot analysis were performed in BMSCs to unravel the underlying molecular mechanism. RESULTS: -OMVs promoted proliferation but inhibited osteogenic differentiation of BMSCs. High-throughput sequencing results showed that serum amyloid A (SAA), especially SAA3, was robustly upregulated in -OMVs-treated BMSCs. Upregulated SAA3 promoted TLR4, MyD88, and NF-κB p65 and inhibited osteogenic differentiation of -OMVs-treated BMSCs. The knockdown of SAA3 in BMSCs downregulated -OMVs-induced TLR4, MyD88, and NF-κB p65 and rescued -OMVs-inhibited osteogenic differentiation. CONCLUSIONS: Our results indicate that -OMVs inhibit osteogenic differentiation of BMSCs via the SAA3-mediated TLR4/MyD88/NF-κB axis, providing novel targets for the treatment of periodontitis-induced alveolar bone loss.

摘要

背景：牙周炎引起的牙槽骨丧失是牙齿缺失的主要原因。（）是牙周炎的主要致病菌。源自（-OMVs）的外膜囊泡（OMVs）含有多种生物活性分子，多项研究表明-OMVs可能参与牙周炎引起的牙槽骨丧失。 材料与方法：分离并鉴定-OMVs。分析-OMVs对骨髓间充质干细胞（BMSCs）增殖和成骨分化的影响。在BMSCs中进行高通量测序、RT-qPCR和蛋白质印迹分析以揭示潜在的分子机制。 结果：-OMVs促进BMSCs的增殖但抑制其成骨分化。高通量测序结果表明，血清淀粉样蛋白A（SAA），尤其是SAA3，在-OMVs处理的BMSCs中显著上调。上调的SAA3促进TLR4、MyD88和NF-κB p65表达，并抑制-OMVs处理的BMSCs的成骨分化。在BMSCs中敲低SAA3可下调-OMVs诱导的TLR4、MyD88和NF-κB p65表达，并挽救-OMVs抑制的成骨分化。 结论：我们的结果表明，-OMVs通过SAA3介导的TLR4/MyD88/NF-κB轴抑制BMSCs的成骨分化，为治疗牙周炎引起的牙槽骨丧失提供了新的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/913c435525f0/ZJOM_A_2540823_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/19000c0d0167/ZJOM_A_2540823_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/6bd55ac3882a/ZJOM_A_2540823_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/2ac7a4e9595d/ZJOM_A_2540823_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/20231af33832/ZJOM_A_2540823_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/25d4e0233fe9/ZJOM_A_2540823_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/6b863df6f591/ZJOM_A_2540823_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/913c435525f0/ZJOM_A_2540823_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/19000c0d0167/ZJOM_A_2540823_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/6bd55ac3882a/ZJOM_A_2540823_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/2ac7a4e9595d/ZJOM_A_2540823_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/20231af33832/ZJOM_A_2540823_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/25d4e0233fe9/ZJOM_A_2540823_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/6b863df6f591/ZJOM_A_2540823_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e25/12337729/913c435525f0/ZJOM_A_2540823_F0007_OC.jpg

相似文献

[1]
OMVs inhibit osteogenic differentiation of BMSCs via SAA3/TLR4/MyD88/NF-κB axis.

J Oral Microbiol. 2025-8-8

[2]
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Biomol Biomed. 2025-4-3

[3]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Porphyromonas gingivalis outer membrane vesicles divert host innate immunity and promote inflammation via C4' monophosphorylated lipid A.

J Immunol. 2025-5-1

[2]
Recent Advances in Studies of Serum Amyloid A: Implications in Inflammation, Immunity and Tumor Metastasis.

Int J Mol Sci. 2025-1-24

[3]
Irisin alleviates obesity-induced bone loss by inhibiting interleukin 6 expression via TLR4/MyD88/NF-κB axis in adipocytes.

J Adv Res. 2025-3

[4]
Gingipain-carrying outer membrane vesicles from Porphyromonas gingivalis cause barrier dysfunction of Caco-2 cells by releasing gingipain into the cytosol.

Biochem Biophys Res Commun. 2024-5-7

[5]
Bacterial Outer Membrane Vesicles: Role in Pathogenesis and Host-Cell Interactions.

Antibiotics (Basel). 2023-12-28

[6]
Toll-like receptor 4 (TLR4): new insight immune and aging.

Immun Ageing. 2023-11-24

[7]
Clinical diagnostic value of IL-14, 1L-16 and SAA in periodontitis.

Clin Oral Investig. 2023-11

[8]
In Situ Raman Study of Neurodegenerated Human Neuroblastoma Cells Exposed to Outer-Membrane Vesicles Isolated from .

Int J Mol Sci. 2023-8-28

[9]
Evaluation of Pentraxin 3 and Serum Amyloid A in the Gingival Crevicular Fluid of Patients with Periodontal Disease and Obesity.

J Clin Med. 2023-5-17

[10]
in the Development of Periodontitis: Impact on Dysbiosis and Inflammation.

Arch Razi Inst. 2022-10

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