首页> 外文期刊>International Journal of Clinical and Experimental Pathology >Mesenchymal stem cell-derived extracellular vesiclespromote apoptosis in RSC96 Schwann cells throughthe activation of the ERK pathway
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Mesenchymal stem cell-derived extracellular vesiclespromote apoptosis in RSC96 Schwann cells throughthe activation of the ERK pathway

机译:通过激活ERK途径使间充质干细胞衍生的RSC96雪旺细胞中的细胞外囊泡浮游细胞凋亡

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Mesenchymal stem cells (MSCs) are known for their capacity to produce extracellular vesicles (EVs), whichare key mediators of information transfer between different cells for tissue repair and regeneration. Schwann cellsare the major glial cells of the peripheral nervous system and play a key role in the survival, function, and regenerationof neurons. However, the action of MSC-derived EVs (MSC-EVs) on Schwann cells remains unclear. In thepresent study, we investigated the effect of rat bone marrow MSC-EVs on RSC96 Schwann cells. EVs derived fromRat bone marrow MSCs were isolated by ultracentrifugation and characterized by transmission electron microscopy(TEM) and scanning electron microscopy (SEM). The effects of MSC-EVs on RSC96 cell proliferation, migration,apoptosis, and the protein levels were analyzed using the MTT and Colony-forming assays, the Transwell and woundhealing assays, flow cytometry, and western blot, respectively. We found that rat MSCs secreted 80-400 nm heterogeneoussmall vesicles, which were defined as EVs. Incubation of RSC96 cells with rat MSC-EVs resulted in the uptakeof EVs by the cells. MSC-EV treatment significantly inhibited RSC96 cell proliferation and migration, promotedtheir apoptosis, and activated the ERK pathway, while ERK signal repression using U0126 exhibited the oppositeeffects. Our data showed that MSC-EVs inhibited proliferation and migration and promoted apoptosis through theactivation of the ERK pathway in RSC96 cells. Thus, the effect of BMSC-EVs on RSC96 cells may affect peripheralnerve injury and repair, as mediated by Schwann cells.
机译:间充质干细胞(MSC)具有产生细胞外囊泡(EVs)的能力,而细胞外囊泡是不同细胞之间信息传递以进行组织修复和再生的关键介质。雪旺氏细胞是周围神经系统的主要神经胶质细胞,在神经元的存活,功能和再生中起关键作用。但是,尚不清楚MSC衍生的电动汽车(MSC-EV)对雪旺细胞的作用。在本研究中,我们研究了大鼠骨髓MSC-EV对RSC96雪旺细胞的作用。通过超速离心分离大鼠骨髓间充质干细胞,并通过透射电子显微镜(TEM)和扫描电子显微镜(SEM)对其进行表征。分别使用MTT和集落形成测定,Transwell和伤口愈合测定,流式细胞术和western印迹分析了MSC-EV对RSC96细胞增殖,迁移,凋亡和蛋白质水平的影响。我们发现大鼠MSC分泌80-400 nm的异质小囊泡,被定义为电动汽车。将RSC96细胞与大鼠MSC-EV一起孵育会导致细胞摄取EV。 MSC-EV处理可显着抑制RSC96细胞的增殖和迁移,促进其凋亡并激活ERK通路,而使用U0126抑制ERK信号则显示相反的效果。我们的数据表明,MSC-EVs通过激活RSC96细胞中的ERK途径抑制增殖和迁移并促进凋亡。因此,BMSC-EV对RSC96细胞的作用可能会影响雪旺细胞介导的周围神经损伤和修复。

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