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外泌体来源于 miRNA-210 过表达的骨髓间充质干细胞,通过 NF-κB 通路保护脂多糖诱导的软骨细胞损伤。

Exosomes derived from miRNA-210 overexpressing bone marrow mesenchymal stem cells protect lipopolysaccharide induced chondrocytes injury via the NF-κB pathway.

机构信息

Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, China; Guangdong Provincial Center for Quality Control of Minimally Invasive Spine Surgery, Guangzhou, Guangdong 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou, Guangdong 510630, China.

Department of Orthopedic Surgery, Shenzhen University General Hospital, Shenzhen, Guangdong 518055, China.

出版信息

Gene. 2020 Aug 15;751:144764. doi: 10.1016/j.gene.2020.144764. Epub 2020 May 16.

DOI:10.1016/j.gene.2020.144764
PMID:32428694
Abstract

Bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (Exos) have anti-inflammatory and anti-apoptotic functions. miRNA-210 has also been confirmed to play a role in inhibiting proinflammatory cytokines. Herein, we aimed to explore the effects of Exos derived from miRNA-210-overexpressing BMSCs (BMSCs-210-Exos) and the mechanisms by which they provide protection to chondrocytes from lipopolysaccharide (LPS)-induced injury. BMSCs were transfected with or without miRNA-210. Exos substantially improved the proliferation of chondrocytes and inhibited LPS-induced cell apoptosis. Furthermore, BMSCs-210-Exos promoted the proliferation of chondrocytes and prevented LPS-induced cell apoptosis better than BMSCs-Exos not overexpressing miRNA-210. In addition, tumor necrosis factor receptor superfamily member 21 (Tnfrsf21) expression was inhibited and the NF-κB pathway was attenuated by both BMSCs-Exos and BMSCs-210-Exos during LPS-induced chondrocyte injury. Collectively, these results suggest that BMSCs-210-Exos enhance the protection of chondrocytes from LPS-induced injury via the NF-κB pathway.

摘要

骨髓间充质干细胞(BMSCs)来源的外泌体(Exos)具有抗炎和抗凋亡作用。miRNA-210 也被证实能抑制促炎细胞因子的产生。在此,我们旨在探讨过表达 miRNA-210 的 BMSCs 来源的外泌体(BMSCs-210-Exos)的作用及其对脂多糖(LPS)诱导的软骨细胞损伤的保护机制。转染 miRNA-210 或不转染 miRNA-210 的 BMSCs。外泌体显著改善了软骨细胞的增殖,并抑制了 LPS 诱导的细胞凋亡。此外,BMSCs-210-Exos 促进软骨细胞增殖和防止 LPS 诱导的细胞凋亡比不表达 miRNA-210 的 BMSCs-Exos 更好。此外,在 LPS 诱导的软骨细胞损伤中,BMSCs-Exos 和 BMSCs-210-Exos 均抑制肿瘤坏死因子受体超家族成员 21(Tnfrsf21)的表达并减弱 NF-κB 通路。综上所述,这些结果表明 BMSCs-210-Exos 通过 NF-κB 通路增强了对 LPS 诱导的软骨细胞损伤的保护作用。

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