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源自CircAkap7修饰的脂肪间充质干细胞的外泌体可预防脑缺血损伤。

Exosomes Derived From CircAkap7-Modified Adipose-Derived Mesenchymal Stem Cells Protect Against Cerebral Ischemic Injury.

作者信息

Xu Limin, Ji Haifeng, Jiang Yufeng, Cai Liying, Lai Xiaoyin, Wu Feifei, Hu Rongguo, Yang Xuelian, Bao Huan, Jiang Mei

机构信息

Department of Clinical Laboratory, Shanghai Gongli Hospital, The Second Military Medical University, Shanghai, China.

Department of Neurology, Shanghai Gongli Hospital, The Second Military Medical University, Shanghai, China.

出版信息

Front Cell Dev Biol. 2020 Oct 2;8:569977. doi: 10.3389/fcell.2020.569977. eCollection 2020.

DOI:10.3389/fcell.2020.569977
PMID:33123535
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7573549/
Abstract

BACKGROUND

Cerebral ischemic injury is a complicated pathological process. Adipose-derived stromal cells (ADSCs) have been used as a therapeutic strategy, with their therapeutic effects chiefly attributed to paracrine action rather than differentiation. Studies have shown that circAkap7 was found to be downregulated in a mouse model of transient middle cerebral artery occlusion (tMCAO).

METHODS

To explore whether exosomes derived from circAkap7-modified ADSCs (exo-circAkap7) have therapeutic effects on cerebral ischemic injury, a mouse model of tMCAO, as well as an model of oxygen and glucose deprivation-reoxygenation (OGD-R) in primary astrocytes, were used.

RESULTS

Results showed that treatment with exo-circAkap7 protected against tMCAO in mice, and experiments confirmed that co-culture with exo-circAkap7 attenuated OGD-R-induced cellular injury by absorbing miR-155-5p, promoting ATG12-mediated autophagy, and inhibiting NRF2-mediated oxidative stress.

CONCLUSION

We demonstrate here that exo-circAkap7 protected against cerebral ischemic injury by promoting autophagy and ameliorating oxidative stress.

摘要

背景

脑缺血损伤是一个复杂的病理过程。脂肪来源的基质细胞（ADSCs）已被用作一种治疗策略，其治疗效果主要归因于旁分泌作用而非分化。研究表明，在短暂性大脑中动脉闭塞（tMCAO）小鼠模型中发现circAkap7表达下调。

方法

为了探究circAkap7修饰的脂肪来源的基质细胞分泌的外泌体（exo-circAkap7）对脑缺血损伤是否具有治疗作用，使用了tMCAO小鼠模型以及原代星形胶质细胞的氧糖剥夺-复氧（OGD-R）模型。

结果

结果显示，exo-circAkap7治疗可保护小鼠免受tMCAO损伤， 实验证实，与exo-circAkap7共培养可通过吸收miR-155-5p、促进ATG12介导的自噬以及抑制NRF2介导的氧化应激来减轻OGD-R诱导的细胞损伤。

结论

我们在此证明，exo-circAkap7通过促进自噬和改善氧化应激来保护免受脑缺血损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ae0/7573549/0aebc5f3381d/fcell-08-569977-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ae0/7573549/04772f0d0865/fcell-08-569977-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ae0/7573549/960a977e0ee2/fcell-08-569977-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ae0/7573549/0aebc5f3381d/fcell-08-569977-g010.jpg

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