微泡
外体
细胞生物学
间充质干细胞
细胞凋亡
PI3K/AKT/mTOR通路
蛋白激酶B
生物
PTEN公司
细胞
细胞生长
信号转导
干细胞
癌症研究
化学
小RNA
生物化学
基因
作者
Hong Wei,Yijuan Xu,Qi Chen,Hui Chen,Xiaolan Zhu,Yuefeng Li
标识
DOI:10.1038/s41419-020-2490-4
摘要
Abstract Hypoxia limits the survival and function of neurons in the development of Alzheimer’s diseases. Exosome-dependent intercellular communication is an emerging signaling mechanism involved in tissue repair and regeneration; however, the effect and underlying mechanism of mesenchymal stem cell-derived exosomes in regulating neuronal cell apoptosis have not been determined. Here, we showed that the establishment of an AD cell model was accompanied by increased HIF-1α expression and cell apoptosis, impaired cell migration, and decreased miR-223. MSC-derived exosomes were internalized by the AD cell coculture model in a time-dependent manner, resulting in reduced cell apoptosis, enhanced cell migration and increased miR-223, and these effects were reversed by KC7F2, a hypoxic inhibitor. Furthermore, MSC-derived exosomal miR-223 inhibited the apoptosis of neurons in vitro by targeting PTEN, thus activating the PI3K/Akt pathway. In addition, exosomes isolated from the serum of AD patients promoted cell apoptosis. In short, our study showed that MSC-derived exosomal miR-223 protected neuronal cells from apoptosis through the PTEN-PI3K/Akt pathway and provided a potential therapeutic approach for AD.
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