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首页> 美国卫生研究院文献>Aging (Albany NY) >Neural stem cell small extracellular vesicle-based delivery of 14-3-3t reduces apoptosis and neuroinflammation following traumatic spinal cord injury by enhancing autophagy by targeting Beclin-1
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Neural stem cell small extracellular vesicle-based delivery of 14-3-3t reduces apoptosis and neuroinflammation following traumatic spinal cord injury by enhancing autophagy by targeting Beclin-1

机译：基于神经干细胞小细胞外囊泡的14-3-3t递送通过靶向Beclin-1增强自噬而减少了脊髓损伤后的细胞凋亡和神经炎症

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Neural stem cell-derived small extracellular vesicles (NSC-sEVs) play an important role in the repair of tissue damage. Our previous in vitro and in vivo studies found that preconditioning with NSC-sEVs promoted the recovery of functional behaviors following spinal cord injury by activating autophagy. However, the underlying mechanisms for such observations remain unclear. In this study, we further explored the mechanisms by which NSC-sEVs repair spinal cord injury via autophagy. We found that NSC-sEVs contain 14-3-3t protein, of which the overexpression or knockdown enhanced and decreased autophagy, respectively. In addition, 14-3-3t overexpression enhanced the anti-apoptotic and anti-inflammatory effects of NSC-sEVs, further promoting functional behavior recovery following spinal cord injury. The overexpression of 14-3-3t was used to further validate the in vivo results through a series of in vitro experiments. Conversely, knockdown of 14-3-3t attenuated the anti-apoptotic and anti-inflammatory effects of NSC-sEVs. Further studies also confirmed that NSC-sEVs increased Beclin-1 expression, with which 14-3-3t interacted and promoted its localization to autophagosome precursors. In this study, we found that NSC-sEVs deliver 14-3-3t, which interacts with Beclin-1 to activate autophagy. Our results indicate that 14-3-3t acts via a newly-discovered mechanism for the activation of autophagy by NSC-sEVs.
机译：神经干细胞衍生的小细胞外囊泡（NSC-sEVs）在修复组织损伤中起重要作用。我们先前的体外和体内研究发现，用NSC-sEV进行预处理可通过激活自噬促进脊髓损伤后功能行为的恢复。但是，这种观察的潜在机制仍不清楚。在这项研究中，我们进一步探讨了NSC-sEVs通过自噬修复脊髓损伤的机制。我们发现NSC-sEVs包含14-3-3t蛋白，其中过表达或敲低分别增强和减少了自噬。此外，14-3-3t过表达增强了NSC-sEV的抗凋亡和抗炎作用，进一步促进了脊髓损伤后功能行为的恢复。通过一系列的体外实验，将14-3-3t的过表达用于进一步验证体内结果。相反，敲除14-3-3t减弱了NSC-sEV的抗凋亡和抗炎作用。进一步的研究还证实，NSC-sEVs可以增加Beclin-1的表达，并与14-3-3t相互作用并促进其定位于自噬体前体。在这项研究中，我们发现NSC-sEV传递的14-3-3t与Beclin-1相互作用以激活自噬。我们的结果表明14-3-3t通过一种新发现的机制起作用，用于激活NSC-sEV的自噬。

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