Microglia-derived exosomes selective sorted by YB-1 alleviate nerve damage and cognitive outcome in Alzheimer's disease release_ktroyltmvjaoxpvr2rd3tiewhy

by Hong Wei, Zhuzhi Zhu, Yuhao Xu, Li Lin, Qi Chen, Yueqin Liu, Yuefeng Li, Xiaolan Zhu

Published in Journal of Translational Medicine by Springer Science and Business Media LLC.

2024   Volume 22, Issue 1, p466

Abstract

<jats:title>Abstract</jats:title><jats:sec> <jats:title>Background</jats:title> Neuroinflammation is a characteristic pathological change of Alzheimer's Diseases (AD). Microglia have been reported to participate in inflammatory responses within the central nervous system. However, the mechanism of microglia released exosome (EXO) contribute to communication within AD microenvironment remains obscure. </jats:sec><jats:sec> <jats:title>Methods</jats:title> The interaction between microglia and AD was investigated in vitro and in vivo. RNA-binding protein immunoprecipitation (RIP) was used to investigate the mechanisms of miR-223 and YB-1. The association between microglia derived exosomal YB-1/miR-223 axis and nerve cell damage were assessed using Western blot, immunofluorescence, RT-PCR, ELISA and wound healing assay. </jats:sec><jats:sec> <jats:title>Results</jats:title> Here, we reported AD model was responsible for the M1-like (pro-inflammatory) polarization of microglia which in turn induced nerve cell damage. While M2-like (anti-inflammatory) microglia could release miR-223-enriched EXO which reduced neuroinflammation and ameliorated nerve damage in AD model in <jats:italic>vivo</jats:italic> and in <jats:italic>vitro</jats:italic>. Moreover, YB-1 directly interacted with miR-223 both in cell and EXO, and participated in microglia exosomal miR-223 loading. </jats:sec><jats:sec> <jats:title>Conclusion</jats:title> These results indicate that anti-inflammatory microglia-mediated neuroprotection form inflammatory damage involves exporting miR-223 via EXO sorted by YB-1. Consequently, YB-1-mediated microglia exosomal sorting of miR-223 improved the nerve cell damage repair, representing a promising therapeutic target for AD. </jats:sec>
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