• Am J Transl Res · Jan 2018

    Exosomes secreted by HUVECs attenuate hypoxia/reoxygenation-induced apoptosis in neural cells by suppressing miR-21-3p.

    • Yuan Jiang, Huan Xie, Wei Tu, Hua Fang, Chenxing Ji, Tengfeng Yan, Hongming Huang, Cong Yu, Qing Hu, Ziyun Gao, and Shigang Lv.
    • Department of Neurosurgery, Second Affiliated Hospital of Nanchang University Nanchang 330006, Jiangxi, P. R. China.
    • Am J Transl Res. 2018 Jan 1; 10 (11): 3529-3541.

    BackgroundRemote ischemic postconditioning (RIPostC) is an effective strategy for preventing key organs from becoming impaired due to an ischemia/reperfusion injury. In the current study, we investigated how remote exosome transfer of microRNAs (miRs) may contribute to the treatment effect of RIPostC on the central nerve system (CNS).MethodsHuman umbilical vein endothelial cells (HUVECs) were subjected to hypoxia/reoxygenation (H/R) and their miR expression profiles were investigated using the microarray method. The pathways associated with dysregulated miRs were analyzed by gene ontology (GO) annotation of the target genes and a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The role played by the most significantly down-regulated miR (miR-21-3p) in the protective effect of HUVEC-derived exosomes on H/R-treated neural cells was further investigated. The pathway mediating the effect of miR-21-3p was then explored by focusing on activity of autophagy-related 12 (ATG12) protein.ResultsThe miR expression profile of HUVECs significantly changed after H/R administration, with 104 miRs becoming upregulated and 249 miRs becoming downregulated. Based on the GO and KEGG analyses, the target genes of 8 selected miRs were involved in multiple biological pathways, including the hippo signaling pathway and longevity regulating pathway. Further studies showed that inhibition of miR-21-3p by HUVEC-derived exosomes or a specific inhibitor could the block apoptotic process in H/R-treated neural cells. Molecular level studies showed that the effect of miR-21-3p inhibition depended on the restored function of ATG12, which resulted in the activation of autophagy and suppression of apoptosis.ConclusionTaken together, these results suggest that H/R caused significant changes of miR expression in exosomes derived from H/R-treated HUVECs, and the exosomes protect neurons against H/R-induced injuries by suppressing miR-21-3p.

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