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骨髓间充质干细胞中 microRNA-202-3p 的过表达通过促进血管生成和抑制炎症改善脑缺血再灌注损伤。

Overexpression of microRNA-202-3p in bone marrow mesenchymal stem cells improves cerebral ischemia-reperfusion injury by promoting angiogenesis and inhibiting inflammation.

机构信息

Department of Rehabilitation, The First Affiliated Hospital of Nanchang University, Nanchang 330006, China.

出版信息

Aging (Albany NY). 2021 Apr 23;13(8):11877-11888. doi: 10.18632/aging.202889.

DOI:10.18632/aging.202889
PMID:33893248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8109138/
Abstract

BACKGROUND

Cerebral ischemia-reperfusion injury (CIRI) can cause brain tissue inflammation, neuronal degeneration, and apoptosis. There is increasing evidence that microRNAs (miRNA) exert neuroprotective effects by regulating the inflammatory process during cerebral ischemia-reperfusion injury. Additionally, it is increasingly acknowledged that neuroinflammation is regulated by Toll-like receptor 4 (TLR4). However, it is unclear whether miRNA can exert its neuroprotective effects by regulating TLR4-mediated inflammation.

METHODS

The effects of BMSCs over-expressing miR-202-3p on CIRI, angiogenesis in midbrain tissue, and the release of inflammatory factors (IFs) in the serum were measured using rat models. We also used SH-SY5Y cells to establish an ischemia-reperfusion cell model. The interaction between miR-202-3p and TLR4 was analyzed by overexpressing miR-202-3p and knocking down TLR4. Knockdown of TLR4 was performed using siRNA.

RESULTS

Overexpression of miR-202-3p in BMSCs could significantly improve brain function and reduce brain damage. Simultaneously, miR-202-3p could significantly promote angiogenesis, increase the expression of vWF and VEGF, and reduce the expression of IFs. When the expression of TLR4 was significantly reduced in SH-SY5Y cells, the expression of IFs increased. Therefore, miRNA-202-3p may interact with TLR4 to modulate inflammation.

CONCLUSION

Our data indicated that miR-202-3p potentially exerts its neuroprotective effects and protects against CIRI by regulating TLR4-mediated inflammation.

摘要

背景

脑缺血再灌注损伤（CIRI）可引起脑组织炎症、神经元变性和细胞凋亡。越来越多的证据表明，microRNAs（miRNA）通过调节脑缺血再灌注损伤过程中的炎症反应发挥神经保护作用。此外，人们越来越认识到神经炎症受 Toll 样受体 4（TLR4）调节。然而，miRNA 是否可以通过调节 TLR4 介导的炎症发挥其神经保护作用尚不清楚。

方法

使用大鼠模型测量骨髓间充质干细胞过表达 miR-202-3p 对 CIRI、中脑组织血管生成和血清中炎症因子（IFs）释放的影响。我们还使用 SH-SY5Y 细胞建立缺血再灌注细胞模型。通过过表达 miR-202-3p 和敲低 TLR4 来分析 miR-202-3p 与 TLR4 之间的相互作用。TLR4 的敲低是通过 siRNA 实现的。

结果

BMSCs 中 miR-202-3p 的过表达可显著改善脑功能并减轻脑损伤。同时，miR-202-3p 可显著促进血管生成，增加 vWF 和 VEGF 的表达，并减少 IFs 的表达。当 SH-SY5Y 细胞中 TLR4 的表达明显降低时，IFs 的表达增加。因此，miRNA-202-3p 可能通过与 TLR4 相互作用来调节炎症。

结论

我们的数据表明，miR-202-3p 通过调节 TLR4 介导的炎症发挥其神经保护作用并保护 CIRI。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/ec031f19940d/aging-13-202889-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/b0a2b61289e0/aging-13-202889-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/2e92b86db7a9/aging-13-202889-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/e93c2faf6bd5/aging-13-202889-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/0680cbbee665/aging-13-202889-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/ec031f19940d/aging-13-202889-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/b0a2b61289e0/aging-13-202889-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/2e92b86db7a9/aging-13-202889-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/e93c2faf6bd5/aging-13-202889-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/0680cbbee665/aging-13-202889-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6078/8109138/ec031f19940d/aging-13-202889-g005.jpg

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