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| 间充质干细胞外泌体通过TGF-β信号通路抑制成骨分化 |
| Mesenchymal stem cell-derived exosomes inhibit osteogenic differentiation through TGF-β signaling pathway |
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| DOI：10.3969/j.issn.1006-7108.2022.07.007 |
| 中文关键词: 间充质干细胞 外泌体 成骨分化 TGF-β信号通路 |
| 英文关键词:mesenchymal stem cell exosome osteogenic differentiation TGF-β signaling pathway |
| 基金项目:湖北省科技厅2019年自然科学基金（2019CFB242） |
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| 中文摘要: |
| 目的 探究间充质干细胞（mesenchymal stem cell，MSC）来源外泌体对MSC成骨分化的影响及其可能的机制。方法 超速离心获得未被地塞米松干预和用地塞米松（10 μmol/L）干预的MSC外泌体：Exo-1和Exo-2。将MSC分为3组：对照组、Exo-1组和Exo-2组，成骨诱导分化培养7 d。生化检测碱性磷酸酶（alkaline phosphatase，ALP）活性。流式检测细胞凋亡率。qRT-PCR检测炎症因子及TGF-β信号通路相关基因表达。Western blot检测TGF-β信号通路相关蛋白表达。结果 用地塞米松干预的MSC来源外泌体能够降低MSC细胞中ALP活性，细胞凋亡率升高，下调NF-κB mRNA表达、Smad3和RUNX2 mRNA和蛋白表达（P＜0.05），上调IL-1β和TNF-α mRNA表达、TGF-β mRNA和蛋白表达（P＜0.05）。结论 用地塞米松（10 μmol/L）干预的MSC来源外泌体能通过TGF-β信号通路抑制MSC成骨分化，促进细胞凋亡和炎症反应。 |
| 英文摘要: |
| Objective To explore the possible mechanism of the effect of mesenchymal stem cell-derived exosomes on osteogenic differentiation of MSC. Methods Exo-1 and EXO-2 of MSC-derived exosomes without or with dexamethasone (10 μmol/L) intervention were obtained by supercentrifugation. MSC was divided into three groups: control group, Exo-1 group, and Exo-2 group. Osteogenic differentiation was induced and cultured for 7 days. Alkaline phosphatase (ALP) activity was determined. The apoptosis rate was detected with flow cytometry. qRT-PCR was used to detect the expression of inflammatory factors and TGF-β signaling pathway related genes. Western blotting was used to detect the expression of TGF-β signaling pathway related proteins. Results MSC-derived exosomes treated with dexamethasone reduced ALP activity and increased apoptosis rate by MSC cells. Dexamethasone-treated MSC-derived exosomes down-regulated the expressions of NF-κB mRNA, Smad3, RUNX2 mRNA and protein (P<0.05), and up-regulated the expression of IL-1 β and TNF- α mRNA, TGF- β mRNA and protein (P<0.05). Conclusion Dexamethasone-treated (10 μmol/L) MSC-derived exosomes inhibit osteogenic differentiation of MSC through TGF-β signaling pathway and promote apoptosis and inflammation. |
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